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Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of <t>VEGF-A</t> expression and <t>VEGF-C</t> expression in tumour cells. The survival rates of patients who had high VEGF-A and VEGF-C expression in tumour cells and patients who had low VEGF-A and VEGF-C expression in tumour cell were 45.1 and 66.6%, respectively. The survival rates of patients who had high VEGF-A and low VEGF-C expression in tumour cells and patients who had low VEGF-A and high VEGF-C expression in tumour cell were 71.6 and 59.7%, respectively.
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Images

1) Product Images from "Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients"

Article Title: Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients

Journal: British Journal of Cancer

doi: 10.1038/sj.bjc.6601992

Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-A expression and VEGF-C expression in tumour cells. The survival rates of patients who had high VEGF-A and VEGF-C expression in tumour cells and patients who had low VEGF-A and VEGF-C expression in tumour cell were 45.1 and 66.6%, respectively. The survival rates of patients who had high VEGF-A and low VEGF-C expression in tumour cells and patients who had low VEGF-A and high VEGF-C expression in tumour cell were 71.6 and 59.7%, respectively.
Figure Legend Snippet: Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-A expression and VEGF-C expression in tumour cells. The survival rates of patients who had high VEGF-A and VEGF-C expression in tumour cells and patients who had low VEGF-A and VEGF-C expression in tumour cell were 45.1 and 66.6%, respectively. The survival rates of patients who had high VEGF-A and low VEGF-C expression in tumour cells and patients who had low VEGF-A and high VEGF-C expression in tumour cell were 71.6 and 59.7%, respectively.

Techniques Used: Expressing

Expression of VEGF-C in NSCLC. Vascular endothelial growth factor C was observed in ( A ) tumour cells and ( B ) stromal macrophages.
Figure Legend Snippet: Expression of VEGF-C in NSCLC. Vascular endothelial growth factor C was observed in ( A ) tumour cells and ( B ) stromal macrophages.

Techniques Used: Expressing

Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-C expression in tumour cells: patients who had high staining for VEGF-C showed significantly less favourable survival rates compared with patients who had low staining for VEGF-C ( P =0.046).
Figure Legend Snippet: Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-C expression in tumour cells: patients who had high staining for VEGF-C showed significantly less favourable survival rates compared with patients who had low staining for VEGF-C ( P =0.046).

Techniques Used: Expressing, Staining

2) Product Images from "Adventitial transduction of lentivirus-shRNA-VEGF-A in arteriovenous fistula reduces venous stenosis formation"

Article Title: Adventitial transduction of lentivirus-shRNA-VEGF-A in arteriovenous fistula reduces venous stenosis formation

Journal: Kidney International

doi: 10.1038/ki.2013.290

Cellular proliferation, matrix metalloproteinase 2 ( MMP-2 ), and matrix metalloproteinase 9 ( MMP-9 ) are decreased in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced vessels. ( a , upper panel) Representative sections after Ki-67 staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled shRNA (control (C)) or Avastin-treated vessels or immunoglobulin G (IgG) controls at days 14 (D14) and 28 (D28). Nuclei staining brown are positive for Ki-67. IgG antibody staining was performed to serve as negative controls. *Indicates the lumen. All are original magnification × 40. Bar=200 μm. Pooled data for the LV and C groups or Avastin-treated vessels or IgG controls are shown in the lower panel. This demonstrates a significant decrease in the mean Ki-67 index in the LV-transduced vessels when compared with the C vessels at day 14 ( P
Figure Legend Snippet: Cellular proliferation, matrix metalloproteinase 2 ( MMP-2 ), and matrix metalloproteinase 9 ( MMP-9 ) are decreased in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced vessels. ( a , upper panel) Representative sections after Ki-67 staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled shRNA (control (C)) or Avastin-treated vessels or immunoglobulin G (IgG) controls at days 14 (D14) and 28 (D28). Nuclei staining brown are positive for Ki-67. IgG antibody staining was performed to serve as negative controls. *Indicates the lumen. All are original magnification × 40. Bar=200 μm. Pooled data for the LV and C groups or Avastin-treated vessels or IgG controls are shown in the lower panel. This demonstrates a significant decrease in the mean Ki-67 index in the LV-transduced vessels when compared with the C vessels at day 14 ( P

Techniques Used: shRNA, Staining

Smooth muscle cell index and vascular endothelial growth factor receptor 1 ( VEGFR-1 ) expression are reduced in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced vessels. ( a , upper panel) Representative sections after α-smooth muscle actin (α-SMA) staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled shRNA (control (C)) and Avastin treated with control vessels at days 14 and 28. Cells staining brown are positive for α-SMA. immunoglobulin G (IgG) antibody staining was performed to serve as negative control. *Indicates the lumen. All are original magnification × 40. Bar=200 μm. Pooled data for the LV and C groups and Avastin-treated and control vessels are shown in a (lower panel). This demonstrates a significant reduction in the average α-SMA index in LV-transduced vessels when compared with C vessels by day 21 ( P
Figure Legend Snippet: Smooth muscle cell index and vascular endothelial growth factor receptor 1 ( VEGFR-1 ) expression are reduced in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced vessels. ( a , upper panel) Representative sections after α-smooth muscle actin (α-SMA) staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled shRNA (control (C)) and Avastin treated with control vessels at days 14 and 28. Cells staining brown are positive for α-SMA. immunoglobulin G (IgG) antibody staining was performed to serve as negative control. *Indicates the lumen. All are original magnification × 40. Bar=200 μm. Pooled data for the LV and C groups and Avastin-treated and control vessels are shown in a (lower panel). This demonstrates a significant reduction in the average α-SMA index in LV-transduced vessels when compared with C vessels by day 21 ( P

Techniques Used: Expressing, shRNA, Staining, Negative Control

Hematoxylin and eosin (H E) and picrosirius red staining of the lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced and Avastin-treated vessels have increased lumen vessel area with decreased media and adventitia area and collagen expression. ( a , first column) Representative sections after H E at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled- VEGF-A (control (C))–transduced vessels or Avastin-treated vessels or immunoglobulin G (IgG) controls at day 14 showing increase in lumen vessel area. ( a , second column) Representative polarized light microscopy of picrosirius red–stained venous stenosis showing decreased fibrosis (collagen fibers are bright yellow) of the LV and C-transduced vessels and Avastin-treated vessels and controls. Qualitatively, there is a reduction in collagen staining by Sirius red by days 3–21. *Indicates the lumen. Bar=200 μm. Pooled data for mean lumen vessel area LV and C groups and Avastin-treated and control vessels are shown in b . There is a significant increase in the mean lumen vessel area in the LV-transduced vessels when compared with C vessels for days 14–28 ( P
Figure Legend Snippet: Hematoxylin and eosin (H E) and picrosirius red staining of the lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced and Avastin-treated vessels have increased lumen vessel area with decreased media and adventitia area and collagen expression. ( a , first column) Representative sections after H E at the venous stenosis of the LV-shRNA- VEGF-A (LV) and scrambled- VEGF-A (control (C))–transduced vessels or Avastin-treated vessels or immunoglobulin G (IgG) controls at day 14 showing increase in lumen vessel area. ( a , second column) Representative polarized light microscopy of picrosirius red–stained venous stenosis showing decreased fibrosis (collagen fibers are bright yellow) of the LV and C-transduced vessels and Avastin-treated vessels and controls. Qualitatively, there is a reduction in collagen staining by Sirius red by days 3–21. *Indicates the lumen. Bar=200 μm. Pooled data for mean lumen vessel area LV and C groups and Avastin-treated and control vessels are shown in b . There is a significant increase in the mean lumen vessel area in the LV-transduced vessels when compared with C vessels for days 14–28 ( P

Techniques Used: Staining, shRNA, Expressing, Light Microscopy

There is decreased proliferation, invasion, α-smooth muscle actin (α-SMA), and matrix metalloproteinase 2 ( MMP-2 ) expression with increased caspase 3 activities in the lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced cells subjected to hypoxia. Western blot for α-SMA after transduction LV-shRNA- VEGF-A (LV) and scrambled shRNA- VEGF-A (C) in AKR-2B fibroblasts subjected to hypoxia at 24 and 72 h. A typical western blot is shown in the upper panel and the pooled data in the lower panel ( a ). This demonstrates a significant reduction in the mean α-SMA expression in the LV-transduced cells when compared with C cells at 24 ( P
Figure Legend Snippet: There is decreased proliferation, invasion, α-smooth muscle actin (α-SMA), and matrix metalloproteinase 2 ( MMP-2 ) expression with increased caspase 3 activities in the lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced cells subjected to hypoxia. Western blot for α-SMA after transduction LV-shRNA- VEGF-A (LV) and scrambled shRNA- VEGF-A (C) in AKR-2B fibroblasts subjected to hypoxia at 24 and 72 h. A typical western blot is shown in the upper panel and the pooled data in the lower panel ( a ). This demonstrates a significant reduction in the mean α-SMA expression in the LV-transduced cells when compared with C cells at 24 ( P

Techniques Used: Expressing, shRNA, Western Blot, Transduction

Cartoon of proposed mechanism. Schematic showing ( a ) normal vein, ( b ) vein after arteriovenous fistula (AVF) placement, and ( c ) outflow vein after fistula placement with lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A ) silencing and its different mechanisms. HIF-1α, hypoxia-inducible factor-1α.
Figure Legend Snippet: Cartoon of proposed mechanism. Schematic showing ( a ) normal vein, ( b ) vein after arteriovenous fistula (AVF) placement, and ( c ) outflow vein after fistula placement with lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A ) silencing and its different mechanisms. HIF-1α, hypoxia-inducible factor-1α.

Techniques Used: shRNA

( a ) Representative sections from TdT-mediated dNTP nick end labeling (TUNEL) staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) with scrambled- VEGF-A (control (C))–transduced control vessels or Avastin-treated with immunoglobulin G (IgG) controls at days 14 and 28. Nuclei staining brown are positive for TUNEL. Negative control is shown where the recombinant terminal deoxynucleotidyl transferase enzyme was omitted. All are original magnification × 40. Bar=200 μm. *Indicates the lumen. Pooled data for LV- and C-transduced vessels or Avastin-treated or IgG controls are shown in b . This demonstrates a significant increase in the mean TUNEL index at day 14 ( P
Figure Legend Snippet: ( a ) Representative sections from TdT-mediated dNTP nick end labeling (TUNEL) staining at the venous stenosis of the LV-shRNA- VEGF-A (LV) with scrambled- VEGF-A (control (C))–transduced control vessels or Avastin-treated with immunoglobulin G (IgG) controls at days 14 and 28. Nuclei staining brown are positive for TUNEL. Negative control is shown where the recombinant terminal deoxynucleotidyl transferase enzyme was omitted. All are original magnification × 40. Bar=200 μm. *Indicates the lumen. Pooled data for LV- and C-transduced vessels or Avastin-treated or IgG controls are shown in b . This demonstrates a significant increase in the mean TUNEL index at day 14 ( P

Techniques Used: End Labeling, TUNEL Assay, Staining, shRNA, Negative Control, Recombinant

Vascular endothelial growth factor-A ( VEGF-A ) expression is reduced in lentivirus (LV)–small hairpin RNA (shRNA)- VEGF-A -transduced and Avastin-treated vessels with decreased CD31 staining. ( a , first to third columns) In situ hybridization of mRNA for VEGF-A in the LV-transduced vessels when compared with scrambled-shRNA- VEGF-A (control (C)) vessels, with arrows on cells positive for VEGF-A mRNA expression (brown). By day 3 (D3), there was a reduction of mRNA for VEGF-A being localized to the media and adventitia and by day 7 (D7), it was localized to the media and intima. In contrast, the vessels transduced with C shRNA showed increased mRNA expression of VEGF-A in the adventitia and media by day 3, and in the media and intima by day 7. ( b ) Pooled data for the in situ transcript levels of VEGF-A in the outflow vein of the LV-transduced vessels that was significantly reduced when compared with C vessels at day 7 ( P
Figure Legend Snippet: Vascular endothelial growth factor-A ( VEGF-A ) expression is reduced in lentivirus (LV)–small hairpin RNA (shRNA)- VEGF-A -transduced and Avastin-treated vessels with decreased CD31 staining. ( a , first to third columns) In situ hybridization of mRNA for VEGF-A in the LV-transduced vessels when compared with scrambled-shRNA- VEGF-A (control (C)) vessels, with arrows on cells positive for VEGF-A mRNA expression (brown). By day 3 (D3), there was a reduction of mRNA for VEGF-A being localized to the media and adventitia and by day 7 (D7), it was localized to the media and intima. In contrast, the vessels transduced with C shRNA showed increased mRNA expression of VEGF-A in the adventitia and media by day 3, and in the media and intima by day 7. ( b ) Pooled data for the in situ transcript levels of VEGF-A in the outflow vein of the LV-transduced vessels that was significantly reduced when compared with C vessels at day 7 ( P

Techniques Used: Expressing, shRNA, Staining, In Situ Hybridization, Transduction, In Situ

There is decreased hypoxia-inducible factor-1α (HIF-1α) expression and staining in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced and Avastin-treated vessels. ( a ) Real-time PCR (RT- PCR) analysis for HIF-1α expression after transduction with LV and control shRNA (C). A typical blot is shown in the upper panel and the pooled data in the lower panel. This demonstrates a significant reduction in average HIF-1α expression in the LV-transduced vessels when compared with C vessels at days 7 (D7; P
Figure Legend Snippet: There is decreased hypoxia-inducible factor-1α (HIF-1α) expression and staining in lentivirus (LV)–small hairpin RNA (shRNA)–vascular endothelial growth factor-A ( VEGF-A )–transduced and Avastin-treated vessels. ( a ) Real-time PCR (RT- PCR) analysis for HIF-1α expression after transduction with LV and control shRNA (C). A typical blot is shown in the upper panel and the pooled data in the lower panel. This demonstrates a significant reduction in average HIF-1α expression in the LV-transduced vessels when compared with C vessels at days 7 (D7; P

Techniques Used: Expressing, Staining, shRNA, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Transduction

3) Product Images from "Investigation of the Prognostic Significance of Vasculogenic Mimicry and Its Inhibition by Sorafenib in Canine Mammary Gland Tumors"

Article Title: Investigation of the Prognostic Significance of Vasculogenic Mimicry and Its Inhibition by Sorafenib in Canine Mammary Gland Tumors

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2019.01445

Graphic representation of the study design. We selected 248 mammary gland tumors from the veterinary pathology service, and samples were evaluated for the presence of vasculogenic mimicry (VM). Then, we performed CD31/PAS double staining to identify VM structures, confirming that samples were positive for VM. Two canine mammary gland tumor cell lines were selected, and an in vitro tubular assay was performed to identify the cellular VM ability. Based on the VEGF-A and VEGFR-2 immunohistochemical analysis, we selected VEGF-A/VEGFR-2 and validated their expression in our tumor group. After confirming the associations of VEGF-A/VEGFR-2 expression with VM, we performed in vitro assays to evaluate the ability of sorafenib (a VEGFR-2 inhibitor) to inhibit VM in vitro .
Figure Legend Snippet: Graphic representation of the study design. We selected 248 mammary gland tumors from the veterinary pathology service, and samples were evaluated for the presence of vasculogenic mimicry (VM). Then, we performed CD31/PAS double staining to identify VM structures, confirming that samples were positive for VM. Two canine mammary gland tumor cell lines were selected, and an in vitro tubular assay was performed to identify the cellular VM ability. Based on the VEGF-A and VEGFR-2 immunohistochemical analysis, we selected VEGF-A/VEGFR-2 and validated their expression in our tumor group. After confirming the associations of VEGF-A/VEGFR-2 expression with VM, we performed in vitro assays to evaluate the ability of sorafenib (a VEGFR-2 inhibitor) to inhibit VM in vitro .

Techniques Used: Double Staining, In Vitro, Immunohistochemistry, Expressing

4) Product Images from "New molecular staging with G-factor supplements TNM classification in gastric cancer: a multicenter collaborative research by the Japan Society for Gastroenterological Carcinogenesis G-Project committee"

Article Title: New molecular staging with G-factor supplements TNM classification in gastric cancer: a multicenter collaborative research by the Japan Society for Gastroenterological Carcinogenesis G-Project committee

Journal: Gastric Cancer

doi: 10.1007/s10120-014-0338-2

Immunohistochemical findings of p53, VEGF-A, VEGF-C, Reg IV, olfactomedin 4, Claudin-18, MMP7, and HER2
Figure Legend Snippet: Immunohistochemical findings of p53, VEGF-A, VEGF-C, Reg IV, olfactomedin 4, Claudin-18, MMP7, and HER2

Techniques Used: Immunohistochemistry

5) Product Images from "Expression of vascular endothelial growth factor C and chemokine receptor CCR7 in gastric carcinoma and their values in predicting lymph node metastasis"

Article Title: Expression of vascular endothelial growth factor C and chemokine receptor CCR7 in gastric carcinoma and their values in predicting lymph node metastasis

Journal: World Journal of Gastroenterology

doi: 10.3748/wjg.v10.i6.783

Expression of VEGF-C was observed mainly in gas-tric carcinoma cells in metastatic lymph node (original magni-fication ×400).
Figure Legend Snippet: Expression of VEGF-C was observed mainly in gas-tric carcinoma cells in metastatic lymph node (original magni-fication ×400).

Techniques Used: Expressing

ROC curve generated from the combination of VEGF-C and CCR7 expression shows area under curve to be 0.83.
Figure Legend Snippet: ROC curve generated from the combination of VEGF-C and CCR7 expression shows area under curve to be 0.83.

Techniques Used: Generated, Expressing

Expression of VEGF-C was observed mainly in the cytoplasm of gastric carcinoma cells (original magnification ×200). A: diffuse gastric carcinoma; B: intestinal gastric carcinoma.
Figure Legend Snippet: Expression of VEGF-C was observed mainly in the cytoplasm of gastric carcinoma cells (original magnification ×200). A: diffuse gastric carcinoma; B: intestinal gastric carcinoma.

Techniques Used: Expressing

6) Product Images from "Selective Therapeutic Targeting of the Anaplastic Lymphoma Kinase With Liposomal siRNA Induces Apoptosis and Inhibits Angiogenesis in Neuroblastoma"

Article Title: Selective Therapeutic Targeting of the Anaplastic Lymphoma Kinase With Liposomal siRNA Induces Apoptosis and Inhibits Angiogenesis in Neuroblastoma

Journal: Molecular Therapy

doi: 10.1038/mt.2011.142

ALK gene silencing by TL[ ALK -siRNA] induces apoptosis and inhibits angiogenesis in vivo . Immunohistochemistry (IHC) and immunofluorescence (IF) staining performed on formalin-fixed and paraffin-embedded tumor sections of SH-SY5Y subcutaneous ( s.c. ) xenografts treated with TL[ ALK -siRNA] and compared with untreated controls, or those treated with free ALK -siRNA and TL[scr-siRNA]. Black bar: 100 µm. White bar in b , c : 50 µm; in d , e : 100 µm. ( a ) IHC staining for ALK on neuroblastoma (NB) xenografts showing a complete ablation of ALK protein by TL[ ALK -siRNA], and a partial downmodulation by free ALK -siRNA. ( b ) IF staining for Ki-67 highlights a dramatic decrease of cell proliferation in tumors treated with TL[ ALK -siRNA]. ( c ) Terminal deoxynucleotidyl transferase-mediated end labeling (TUNEL) staining remarks a massive induction of apoptosis by TL[ ALK -siRNA] treatment. ( d , e ) Endothelial (CD34) and perivascular [smooth muscle actin (SMA)] cell staining, respectively, after ALK silencing by TL[ ALK -siRNA] in xenograft tumor reveals a strong antiangiogenic effect. On the right side, percentage of positive cells for each specific marker are reported on y-axis of graphs as the mean ± 95% confidence interval (CI) of nine randomly selected fields every three sections of different tumor areas. * P
Figure Legend Snippet: ALK gene silencing by TL[ ALK -siRNA] induces apoptosis and inhibits angiogenesis in vivo . Immunohistochemistry (IHC) and immunofluorescence (IF) staining performed on formalin-fixed and paraffin-embedded tumor sections of SH-SY5Y subcutaneous ( s.c. ) xenografts treated with TL[ ALK -siRNA] and compared with untreated controls, or those treated with free ALK -siRNA and TL[scr-siRNA]. Black bar: 100 µm. White bar in b , c : 50 µm; in d , e : 100 µm. ( a ) IHC staining for ALK on neuroblastoma (NB) xenografts showing a complete ablation of ALK protein by TL[ ALK -siRNA], and a partial downmodulation by free ALK -siRNA. ( b ) IF staining for Ki-67 highlights a dramatic decrease of cell proliferation in tumors treated with TL[ ALK -siRNA]. ( c ) Terminal deoxynucleotidyl transferase-mediated end labeling (TUNEL) staining remarks a massive induction of apoptosis by TL[ ALK -siRNA] treatment. ( d , e ) Endothelial (CD34) and perivascular [smooth muscle actin (SMA)] cell staining, respectively, after ALK silencing by TL[ ALK -siRNA] in xenograft tumor reveals a strong antiangiogenic effect. On the right side, percentage of positive cells for each specific marker are reported on y-axis of graphs as the mean ± 95% confidence interval (CI) of nine randomly selected fields every three sections of different tumor areas. * P

Techniques Used: In Vivo, Immunohistochemistry, Immunofluorescence, Staining, End Labeling, TUNEL Assay, Marker

7) Product Images from "New molecular staging with G-factor supplements TNM classification in gastric cancer: a multicenter collaborative research by the Japan Society for Gastroenterological Carcinogenesis G-Project committee"

Article Title: New molecular staging with G-factor supplements TNM classification in gastric cancer: a multicenter collaborative research by the Japan Society for Gastroenterological Carcinogenesis G-Project committee

Journal: Gastric Cancer

doi: 10.1007/s10120-014-0338-2

Immunohistochemical findings of p53, VEGF-A, VEGF-C, Reg IV, olfactomedin 4, Claudin-18, MMP7, and HER2
Figure Legend Snippet: Immunohistochemical findings of p53, VEGF-A, VEGF-C, Reg IV, olfactomedin 4, Claudin-18, MMP7, and HER2

Techniques Used: Immunohistochemistry

8) Product Images from "Activin-A signaling promotes epithelial–mesenchymal transition, invasion, and metastatic growth of breast cancer"

Article Title: Activin-A signaling promotes epithelial–mesenchymal transition, invasion, and metastatic growth of breast cancer

Journal: NPJ Breast Cancer

doi: 10.1038/npjbcancer.2015.7

Activin promotes tumorigenicity of breast cancer cells in immunocompromised mice. ( a ) Stable overexpression of activin-A in MCF-7 enhances (i), whereas stable knockdown of activin-A in MDA-MB-231 cells (ii) reduces their tumor-forming ability in nude mice. Shown below are the representative images of the tumors formed s.c. ( b ) Immunohistochemical analysis of MCF-7-overexpressing tumors shows EMT-like changes and higher ki-67 index. ( c ) Treatment of MCF-7 cells with activin-A (i) or overexpression of activin-A in MCF-7 cells (ii) results in increased levels of vascular endothelial growth factor-A (VEGF-A). ( d ) Luciferase reporter assay in HEK 293T cells shows that activin-A regulates VEGF promoter activity. ( e ) Tail vein injection of activin-A-overexpressing MCF-7 cells shows better tumor-forming ability in the livers of nude mice (i). Normal is shown here as the reference from an animal without injection of any cells. The panel below (ii) shows the hematoxylin and eosin (H E) staining of the liver tissue sections. The graph (iii) and (iv) shows number and size of nodules formed in the liver per animal. ( f ) CD44 high/ CD24 low fluorescence-activated cell sorting (FACS) analysis of activin-A-overexpressing or knockdown cells shows that activin-A influences stemness of breast cancer cells (i). Quantitative PCR analysis shows that treatment of MCF-7 or MDA-MB-231 cells with recombinant activin-A induces various markers of stemness (ii).
Figure Legend Snippet: Activin promotes tumorigenicity of breast cancer cells in immunocompromised mice. ( a ) Stable overexpression of activin-A in MCF-7 enhances (i), whereas stable knockdown of activin-A in MDA-MB-231 cells (ii) reduces their tumor-forming ability in nude mice. Shown below are the representative images of the tumors formed s.c. ( b ) Immunohistochemical analysis of MCF-7-overexpressing tumors shows EMT-like changes and higher ki-67 index. ( c ) Treatment of MCF-7 cells with activin-A (i) or overexpression of activin-A in MCF-7 cells (ii) results in increased levels of vascular endothelial growth factor-A (VEGF-A). ( d ) Luciferase reporter assay in HEK 293T cells shows that activin-A regulates VEGF promoter activity. ( e ) Tail vein injection of activin-A-overexpressing MCF-7 cells shows better tumor-forming ability in the livers of nude mice (i). Normal is shown here as the reference from an animal without injection of any cells. The panel below (ii) shows the hematoxylin and eosin (H E) staining of the liver tissue sections. The graph (iii) and (iv) shows number and size of nodules formed in the liver per animal. ( f ) CD44 high/ CD24 low fluorescence-activated cell sorting (FACS) analysis of activin-A-overexpressing or knockdown cells shows that activin-A influences stemness of breast cancer cells (i). Quantitative PCR analysis shows that treatment of MCF-7 or MDA-MB-231 cells with recombinant activin-A induces various markers of stemness (ii).

Techniques Used: Mouse Assay, Over Expression, Multiple Displacement Amplification, Immunohistochemistry, Luciferase, Reporter Assay, Activity Assay, Injection, Staining, Fluorescence, FACS, Real-time Polymerase Chain Reaction, Recombinant

9) Product Images from "Induction of Ischemic Tolerance Protects the Retina From Diabetic Retinopathy"

Article Title: Induction of Ischemic Tolerance Protects the Retina From Diabetic Retinopathy

Journal: The American Journal of Pathology

doi: 10.1016/j.ajpath.2011.01.040

Retinal VEGF levels assessed using Western blot analysis and IHC. A: Representative Western blot analysis performed 6 weeks after the injection of streptozotocin at 24 hours and 3 and 7 days after the sixth ischemia pulse. B: Densitometric analysis of all samples. VEGF levels significantly increased in retinas from diabetic eyes submitted to a sham procedure compared with age-matched controls. This increase was partially prevented at 3 and 7 days (but not 24 hours) after the sixth ischemia pulse. Lower panel: Localization of VEGF protein in retinal sections assessed 6 weeks after the injection of vehicle or streptozotocin. In control retinas ( C ), a weak immunoreactivity was diffusely observed throughout the inner retina. In retinas from diabetic rats submitted to a sham procedure, intense immunoreactive perikarya in GCL cells ( D, arrows ) and in some cells in the inner nuclear layer (INL) ( arrowheads ) were observed. A slight immunoreactivity for VEGF was also observed in the outer retina. The weakly application of ischemia pulses prevented this effect, and only moderate VEGF immunoreactivity was found in the inner retina ( E ). No immunoreactivity was detected in the staining without primary antibody (data not shown). Scale bar = 50 μm ( C–E ). IPL, inner plexiform layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors. Data are the mean ± SEM ( n = 4 eyes per group); * P
Figure Legend Snippet: Retinal VEGF levels assessed using Western blot analysis and IHC. A: Representative Western blot analysis performed 6 weeks after the injection of streptozotocin at 24 hours and 3 and 7 days after the sixth ischemia pulse. B: Densitometric analysis of all samples. VEGF levels significantly increased in retinas from diabetic eyes submitted to a sham procedure compared with age-matched controls. This increase was partially prevented at 3 and 7 days (but not 24 hours) after the sixth ischemia pulse. Lower panel: Localization of VEGF protein in retinal sections assessed 6 weeks after the injection of vehicle or streptozotocin. In control retinas ( C ), a weak immunoreactivity was diffusely observed throughout the inner retina. In retinas from diabetic rats submitted to a sham procedure, intense immunoreactive perikarya in GCL cells ( D, arrows ) and in some cells in the inner nuclear layer (INL) ( arrowheads ) were observed. A slight immunoreactivity for VEGF was also observed in the outer retina. The weakly application of ischemia pulses prevented this effect, and only moderate VEGF immunoreactivity was found in the inner retina ( E ). No immunoreactivity was detected in the staining without primary antibody (data not shown). Scale bar = 50 μm ( C–E ). IPL, inner plexiform layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors. Data are the mean ± SEM ( n = 4 eyes per group); * P

Techniques Used: Western Blot, Immunohistochemistry, Injection, Staining

Retinal histologic examination after 10 weeks of diabetes. Representative photomicrographs of retinal sections from a control eye ( A ) and a diabetic eye without ( B ) or with ( C ) pulses of ischemia. No evident alterations in retinal morphologic features were observed. Immunohistochemical detection of NeuN-positive neurons in the GCL from a control eye ( D ) and a diabetic eye without ( E ) or with ( F ) ischemia pulses. A strong NeuN immunostaining was confined to ganglion cells in the GCL (red). Cell nuclei were counterstained with DAPI (blue). Cell count in the GCL evaluated by hematoxylin-eosin staining, DAPI staining, and NeuN immunostaining ( G ). No differences in the number of cells were observed by these methods. Retinal layer thickness assessed in different groups after 10 weeks of diabetes ( H ). Whole retina thickness was 137.5 ± 12.3 μm, 158.2 ± 10.8 μm, and 152.0 ± 19.2 μm in control, diabetic, and diabetic with ischemia pulses groups, respectively. These values did not differ among groups. Scale bar: 50 μm ( upper ); 100 μm ( middle ). Data are the mean ± SEM ( n = 5 eyes per group). IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors.
Figure Legend Snippet: Retinal histologic examination after 10 weeks of diabetes. Representative photomicrographs of retinal sections from a control eye ( A ) and a diabetic eye without ( B ) or with ( C ) pulses of ischemia. No evident alterations in retinal morphologic features were observed. Immunohistochemical detection of NeuN-positive neurons in the GCL from a control eye ( D ) and a diabetic eye without ( E ) or with ( F ) ischemia pulses. A strong NeuN immunostaining was confined to ganglion cells in the GCL (red). Cell nuclei were counterstained with DAPI (blue). Cell count in the GCL evaluated by hematoxylin-eosin staining, DAPI staining, and NeuN immunostaining ( G ). No differences in the number of cells were observed by these methods. Retinal layer thickness assessed in different groups after 10 weeks of diabetes ( H ). Whole retina thickness was 137.5 ± 12.3 μm, 158.2 ± 10.8 μm, and 152.0 ± 19.2 μm in control, diabetic, and diabetic with ischemia pulses groups, respectively. These values did not differ among groups. Scale bar: 50 μm ( upper ); 100 μm ( middle ). Data are the mean ± SEM ( n = 5 eyes per group). IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors.

Techniques Used: Immunohistochemistry, Immunostaining, Cell Counting, Staining

10) Product Images from "HIF-1? and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia"

Article Title: HIF-1? and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia

Journal: International Journal of Clinical and Experimental Pathology

doi:

Thrombosis area; (A) Degenerating red blood cells and aggregated platelets embedded in a fibrin mesh (H E, 400 x magnification). (B) extracellular CD31 staining in the loose fibrin meshwork (400 x magnification). (C) A few cells stained with an anti-CD68 antibody (400 x magnification). (D, E) A few cells positive for (D) MCT and (E) HIF-1α (400 x magnification). (F) VEGF was expressed in most mononuclear cells (400 x magnification).
Figure Legend Snippet: Thrombosis area; (A) Degenerating red blood cells and aggregated platelets embedded in a fibrin mesh (H E, 400 x magnification). (B) extracellular CD31 staining in the loose fibrin meshwork (400 x magnification). (C) A few cells stained with an anti-CD68 antibody (400 x magnification). (D, E) A few cells positive for (D) MCT and (E) HIF-1α (400 x magnification). (F) VEGF was expressed in most mononuclear cells (400 x magnification).

Techniques Used: Staining

IPEH area; A: Numerous papillae with cellular cores containing mononuclear and endothelial cells (blue arrowhead) and acellular hyalinized cores (red arrow) covered with a flattened endothelium (H E, 400 x magnification). B: Flattened endothelial cells covering the papillae were positive for CD31. Development of an impending acellular papilla from the cellular papilla was also observed (400 x magnification, in the green circle). C, D: Both CD68 and MCT were expressed in a few cells within the core of the cellular papillae but not in the acellular core (400 x magnification). E, F: HIF-1α and VEGF were highly expressed within the cellular core but were absent in the acellular core (400 x magnification).
Figure Legend Snippet: IPEH area; A: Numerous papillae with cellular cores containing mononuclear and endothelial cells (blue arrowhead) and acellular hyalinized cores (red arrow) covered with a flattened endothelium (H E, 400 x magnification). B: Flattened endothelial cells covering the papillae were positive for CD31. Development of an impending acellular papilla from the cellular papilla was also observed (400 x magnification, in the green circle). C, D: Both CD68 and MCT were expressed in a few cells within the core of the cellular papillae but not in the acellular core (400 x magnification). E, F: HIF-1α and VEGF were highly expressed within the cellular core but were absent in the acellular core (400 x magnification).

Techniques Used:

Organizing area; A: Many inflammatory cells infiltrated the perivascular area (H E, 400 x magnification). B: Endothelial cells forming vascular structure were positive for CD31 (400 x magnification). C: Several CD68-positive cells were observed (400 x magnification). D: A few cells positive for MCT, many of which showed degranulation (400 x magnification). E, F: Both HIF-1α and VEGF were highly expressed. HIF-1α was expressed in the majority of mononuclear cells but not in the endothelial cells. On the other hand, VEGF was expressed in both the mononuclear and endothelial cells (400 x magnification).
Figure Legend Snippet: Organizing area; A: Many inflammatory cells infiltrated the perivascular area (H E, 400 x magnification). B: Endothelial cells forming vascular structure were positive for CD31 (400 x magnification). C: Several CD68-positive cells were observed (400 x magnification). D: A few cells positive for MCT, many of which showed degranulation (400 x magnification). E, F: Both HIF-1α and VEGF were highly expressed. HIF-1α was expressed in the majority of mononuclear cells but not in the endothelial cells. On the other hand, VEGF was expressed in both the mononuclear and endothelial cells (400 x magnification).

Techniques Used:

11) Product Images from "Epithelioid Sarcoma and Unclassified Sarcoma with Epithelioid Features: Clinicopathological Variables, Molecular Markers, and a New Experimental Model"

Article Title: Epithelioid Sarcoma and Unclassified Sarcoma with Epithelioid Features: Clinicopathological Variables, Molecular Markers, and a New Experimental Model

Journal: The Oncologist

doi: 10.1634/theoncologist.2010-0174

Biomarker expression in ES and USEF. Immunohistochemical images depicting representative marker expression in human ES and USEF samples included in the tissue microarray. All original images were captured at 200× magnification. Abbreviations: INI-1, integrase interactor 1; EMA, epithelial membrane antigen; ES, epithelioid sarcoma; USEF, unclassified sarcoma with epithelioid features.
Figure Legend Snippet: Biomarker expression in ES and USEF. Immunohistochemical images depicting representative marker expression in human ES and USEF samples included in the tissue microarray. All original images were captured at 200× magnification. Abbreviations: INI-1, integrase interactor 1; EMA, epithelial membrane antigen; ES, epithelioid sarcoma; USEF, unclassified sarcoma with epithelioid features.

Techniques Used: Biomarker Assay, Expressing, Immunohistochemistry, Marker, Microarray

Characterization of the human ES cell lines Epi-544 and VAESBJ. (A): H E, pan-cytokeratin, and vimentin immunohistochemical staining of the original human sample from which Epi-544 was derived. (B): Panel (from top) depicting cell morphology, karyotype, growth in soft agar, migration, and invasion. (C): ES cells do not express INI-1 protein (Western blot, upper panel) or mRNA (RT-PCR; lower panel) in contrast to NHFs and the leiomyosarcoma cell line SKLMS1, which were used as controls. (D): Epi-544 and VAESBJ preserve ES characteristics in vivo. Immunohistochemical staining of tumor xenografts is depicted (inset represents an INI-1 + soft tissue sarcoma xenograft). Abbreviations: H E, hematoxylin and eosin; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; INI-1, integrase interactor 1; EMA, epithelial membrane antigen; ES, epithelioid sarcoma; NHF, normal human fibroblast; USEF, unclassified sarcoma with epithelioid features.
Figure Legend Snippet: Characterization of the human ES cell lines Epi-544 and VAESBJ. (A): H E, pan-cytokeratin, and vimentin immunohistochemical staining of the original human sample from which Epi-544 was derived. (B): Panel (from top) depicting cell morphology, karyotype, growth in soft agar, migration, and invasion. (C): ES cells do not express INI-1 protein (Western blot, upper panel) or mRNA (RT-PCR; lower panel) in contrast to NHFs and the leiomyosarcoma cell line SKLMS1, which were used as controls. (D): Epi-544 and VAESBJ preserve ES characteristics in vivo. Immunohistochemical staining of tumor xenografts is depicted (inset represents an INI-1 + soft tissue sarcoma xenograft). Abbreviations: H E, hematoxylin and eosin; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; INI-1, integrase interactor 1; EMA, epithelial membrane antigen; ES, epithelioid sarcoma; NHF, normal human fibroblast; USEF, unclassified sarcoma with epithelioid features.

Techniques Used: Immunohistochemistry, Staining, Derivative Assay, Migration, Western Blot, Reverse Transcription Polymerase Chain Reaction, In Vivo

12) Product Images from "Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis"

Article Title: Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis

Journal: Scientific Reports

doi: 10.1038/s41598-017-05624-2

Proposed schema for the development of peritoneal fibrosis regulated by CTGF. CTGF contributes to multiple processes fundamentally involved in the pathogenesis of peritoneal fibrosis, including the induction of fibroblast proliferation, myofibroblast differentiation, MMT and VEGF-A production, in an autocrine and/or paracrine manner. Targeting CTGF using FG-3019 may therefore be an effective therapeutic strategy for peritoneal fibrosis.
Figure Legend Snippet: Proposed schema for the development of peritoneal fibrosis regulated by CTGF. CTGF contributes to multiple processes fundamentally involved in the pathogenesis of peritoneal fibrosis, including the induction of fibroblast proliferation, myofibroblast differentiation, MMT and VEGF-A production, in an autocrine and/or paracrine manner. Targeting CTGF using FG-3019 may therefore be an effective therapeutic strategy for peritoneal fibrosis.

Techniques Used:

CG-induced peritoneal angiogenesis and VEGF-A expression required CTGF. ( a ) The localization of CD31 + vessels in fibrotic peritoneum. Peritoneal sections at day 21 were obtained from mice treated with control IgG or FG-3019. Representative tissue sections stained with anti-CD31 antibody are shown. Bars, 50 μm. ( b ) Numbers of CD31 + vessels in the peritoneum are expressed as the mean number ± SEM per HPF (n = 5 mice/group). ( c ) Immunostainings of VEGF-A + cells in fibrotic peritoneum at day 21. Representative tissue sections stained with anti-VEGF-A antibody are shown. Bars, 50 μm. ( d ) Numbers of VEGF-A + vessels in the peritoneum are expressed as the mean number ± SEM per HPF (n = 5 mice/group). ( e ) Representative tissue sections of dual-immunostainings of GFP (green) and VEGF-A (red) at 21 days. Bars, 50 μm. ( f ) VEGF-A expression in PMCs stimulated with 5 ng/ml TGF-β 1 . ( g ) VEGF-A expression in PMCs. PMCs were transfected with control siRNA or CTGF siRNA, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( h ) VEGF-A expression in PMCs. PMCs were preincubated with FG-3019 (10 μg/ml) or control IgG (10 μg/ml) for 1 h, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( i ) VEGF-A expression in NIH3T3 cells stimulated with 5 ng/ml TGF-β 1 . ( j ) VEGF-A expression in NIH3T3 cells. NIH3T3 cells were transfected with control siRNA or CTGF siRNA, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( k ) NIH3T3 cells were preincubated with FG-3019 (10 μg/ml) or control IgG (10 μg/ml) for 1 h, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). In in vitro studies, all data are expressed as copies of VEGF-A mRNA relative to copies of β 2 microglobulin mRNA ± SEM (n = 3 cell preparations/group).
Figure Legend Snippet: CG-induced peritoneal angiogenesis and VEGF-A expression required CTGF. ( a ) The localization of CD31 + vessels in fibrotic peritoneum. Peritoneal sections at day 21 were obtained from mice treated with control IgG or FG-3019. Representative tissue sections stained with anti-CD31 antibody are shown. Bars, 50 μm. ( b ) Numbers of CD31 + vessels in the peritoneum are expressed as the mean number ± SEM per HPF (n = 5 mice/group). ( c ) Immunostainings of VEGF-A + cells in fibrotic peritoneum at day 21. Representative tissue sections stained with anti-VEGF-A antibody are shown. Bars, 50 μm. ( d ) Numbers of VEGF-A + vessels in the peritoneum are expressed as the mean number ± SEM per HPF (n = 5 mice/group). ( e ) Representative tissue sections of dual-immunostainings of GFP (green) and VEGF-A (red) at 21 days. Bars, 50 μm. ( f ) VEGF-A expression in PMCs stimulated with 5 ng/ml TGF-β 1 . ( g ) VEGF-A expression in PMCs. PMCs were transfected with control siRNA or CTGF siRNA, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( h ) VEGF-A expression in PMCs. PMCs were preincubated with FG-3019 (10 μg/ml) or control IgG (10 μg/ml) for 1 h, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( i ) VEGF-A expression in NIH3T3 cells stimulated with 5 ng/ml TGF-β 1 . ( j ) VEGF-A expression in NIH3T3 cells. NIH3T3 cells were transfected with control siRNA or CTGF siRNA, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). ( k ) NIH3T3 cells were preincubated with FG-3019 (10 μg/ml) or control IgG (10 μg/ml) for 1 h, and then stimulated with TGF-β 1 (5 ng/ml for 24 hrs). In in vitro studies, all data are expressed as copies of VEGF-A mRNA relative to copies of β 2 microglobulin mRNA ± SEM (n = 3 cell preparations/group).

Techniques Used: Expressing, Mouse Assay, Staining, Transfection, In Vitro

13) Product Images from "Histopathological findings in systemic sclerosis-related myopathy: fibrosis and microangiopathy with lack of cellular inflammation"

Article Title: Histopathological findings in systemic sclerosis-related myopathy: fibrosis and microangiopathy with lack of cellular inflammation

Journal: Therapeutic Advances in Musculoskeletal Disease

doi: 10.1177/1759720X16671928

Immunohistology (top) and relative quantitative analysis (bottom) of CD31 (left), VEGF-A, VEGF-A 165b (middle) and Coll-I, TGF-β-A (right) in NIM, IIM and SSc groups, respectively. CD31 + vessels (arrows) are abundant and surrounding myofibers in
Figure Legend Snippet: Immunohistology (top) and relative quantitative analysis (bottom) of CD31 (left), VEGF-A, VEGF-A 165b (middle) and Coll-I, TGF-β-A (right) in NIM, IIM and SSc groups, respectively. CD31 + vessels (arrows) are abundant and surrounding myofibers in

Techniques Used:

14) Product Images from "The Features of the Synovium in Early Rheumatoid Arthritis According to the 2010 ACR/EULAR Classification Criteria"

Article Title: The Features of the Synovium in Early Rheumatoid Arthritis According to the 2010 ACR/EULAR Classification Criteria

Journal: PLoS ONE

doi: 10.1371/journal.pone.0036668

Synovial tissue expression of different cellular markers. Synovial tissue expression of, CD55+ fibroblast-like synoviocytes (FLS), CD3+ T CD68+ macrophages, CD3+ T cells, CD22+ B cells, CD138+ plasma cells. A:RA patient according to the 1987 ACR criteria, B:RA patient according to the 2010 ACR/EULAR criteria.
Figure Legend Snippet: Synovial tissue expression of different cellular markers. Synovial tissue expression of, CD55+ fibroblast-like synoviocytes (FLS), CD3+ T CD68+ macrophages, CD3+ T cells, CD22+ B cells, CD138+ plasma cells. A:RA patient according to the 1987 ACR criteria, B:RA patient according to the 2010 ACR/EULAR criteria.

Techniques Used: Expressing

15) Product Images from "Morphoproteomic analysis reveals an overexpressed and constitutively activated phospholipase D1-mTORC2 pathway in endometrial carcinoma"

Article Title: Morphoproteomic analysis reveals an overexpressed and constitutively activated phospholipase D1-mTORC2 pathway in endometrial carcinoma

Journal: International Journal of Clinical and Experimental Pathology

doi:

Expression of PLD1 in endometrial carcinoma (ECa), proliferative-phase endometrium (PE), and secretory-phase endometrium (SE). Isoform-specific antibodies against PLD1 show chromogenic signals in both cytoplasm and nucleoli in both non-neoplastic and neoplastic epithelial cells but with relative cytoplasmic overexpression in the ECa. Original magnification × 400.
Figure Legend Snippet: Expression of PLD1 in endometrial carcinoma (ECa), proliferative-phase endometrium (PE), and secretory-phase endometrium (SE). Isoform-specific antibodies against PLD1 show chromogenic signals in both cytoplasm and nucleoli in both non-neoplastic and neoplastic epithelial cells but with relative cytoplasmic overexpression in the ECa. Original magnification × 400.

Techniques Used: Expressing, Over Expression

16) Product Images from "Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis"

Article Title: Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-017-1241-5

Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm
Figure Legend Snippet: Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm

Techniques Used: Immunohistochemistry, Formalin-fixed Paraffin-Embedded

Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )
Figure Legend Snippet: Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )

Techniques Used:

Correlation between SCP3 and VEGF-C or VEGF-D expressions in human lung cancer cells. a Western blot analysis to characterize the expression of SCP3, VEGF-C and VEGF-D in various human lung adenocarcinoma cells; H146, H460, H1299, H1666, H2228, H358, and H3122. b A plot graph demonstrating the linear relationship between expressing SCP3 (x-axis) and VEGF-C or VEGF-D (y-axis). Western blot analysis of SCP3 expression in lung cancer cell lines cells retrovirally transduced with a pMSCV vector encoding SCP3. c siGFP - or siScp3 transfected with H1299 d H358 and H1666 cells, retrovirally transduced with PMSCV vector encoding either no insert (H358/no insert, H1666/no insert) or Scp3 (H358/SCP3, H1666/SCP3), were incubated in 0.1% FBS-containing DMEM medium for 24 h
Figure Legend Snippet: Correlation between SCP3 and VEGF-C or VEGF-D expressions in human lung cancer cells. a Western blot analysis to characterize the expression of SCP3, VEGF-C and VEGF-D in various human lung adenocarcinoma cells; H146, H460, H1299, H1666, H2228, H358, and H3122. b A plot graph demonstrating the linear relationship between expressing SCP3 (x-axis) and VEGF-C or VEGF-D (y-axis). Western blot analysis of SCP3 expression in lung cancer cell lines cells retrovirally transduced with a pMSCV vector encoding SCP3. c siGFP - or siScp3 transfected with H1299 d H358 and H1666 cells, retrovirally transduced with PMSCV vector encoding either no insert (H358/no insert, H1666/no insert) or Scp3 (H358/SCP3, H1666/SCP3), were incubated in 0.1% FBS-containing DMEM medium for 24 h

Techniques Used: Western Blot, Expressing, Transduction, Plasmid Preparation, Transfection, Incubation

17) Product Images from "Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis"

Article Title: Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-017-1241-5

Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm
Figure Legend Snippet: Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm

Techniques Used: Immunohistochemistry, Formalin-fixed Paraffin-Embedded

Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )
Figure Legend Snippet: Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )

Techniques Used:

Correlation between SCP3 and VEGF-C or VEGF-D expressions in human lung cancer cells. a Western blot analysis to characterize the expression of SCP3, VEGF-C and VEGF-D in various human lung adenocarcinoma cells; H146, H460, H1299, H1666, H2228, H358, and H3122. b A plot graph demonstrating the linear relationship between expressing SCP3 (x-axis) and VEGF-C or VEGF-D (y-axis). Western blot analysis of SCP3 expression in lung cancer cell lines cells retrovirally transduced with a pMSCV vector encoding SCP3. c siGFP - or siScp3 transfected with H1299 d H358 and H1666 cells, retrovirally transduced with PMSCV vector encoding either no insert (H358/no insert, H1666/no insert) or Scp3 (H358/SCP3, H1666/SCP3), were incubated in 0.1% FBS-containing DMEM medium for 24 h
Figure Legend Snippet: Correlation between SCP3 and VEGF-C or VEGF-D expressions in human lung cancer cells. a Western blot analysis to characterize the expression of SCP3, VEGF-C and VEGF-D in various human lung adenocarcinoma cells; H146, H460, H1299, H1666, H2228, H358, and H3122. b A plot graph demonstrating the linear relationship between expressing SCP3 (x-axis) and VEGF-C or VEGF-D (y-axis). Western blot analysis of SCP3 expression in lung cancer cell lines cells retrovirally transduced with a pMSCV vector encoding SCP3. c siGFP - or siScp3 transfected with H1299 d H358 and H1666 cells, retrovirally transduced with PMSCV vector encoding either no insert (H358/no insert, H1666/no insert) or Scp3 (H358/SCP3, H1666/SCP3), were incubated in 0.1% FBS-containing DMEM medium for 24 h

Techniques Used: Western Blot, Expressing, Transduction, Plasmid Preparation, Transfection, Incubation

18) Product Images from "Sialyl Lewis X Expression and Lymphatic Microvessel Density in Primary Tumors of Node-negative Colorectal Cancer Patients Predict Disease Recurrence"

Article Title: Sialyl Lewis X Expression and Lymphatic Microvessel Density in Primary Tumors of Node-negative Colorectal Cancer Patients Predict Disease Recurrence

Journal: Cancer Microenvironment

doi: 10.1007/s12307-008-0014-3

CSLEX1, VEGF-C and VEGF-D expression in colorectal tumors. A tumor negatively stained ( a ) and positively stained ( b ) for CSLEX1; this tumor showed both membrane and cytoplasmic brown staining. A tumor with negative ( c ) and positive cytoplasmic brown staining ( d ) for VEGF-C; similar faint cytoplasmic brown staining as shown in negatively stained tumors for VEGF-C was seen in phosphate buffered saline controles for the VEGF-C staining; this background staining could be clearly differentiated from positive cytoplasmic brown staining for VEGF-C. A tumor with negative ( e ) and positive cytoplasmic brown staining ( f ) for VEGF-D; a brown stromal background staining was seen
Figure Legend Snippet: CSLEX1, VEGF-C and VEGF-D expression in colorectal tumors. A tumor negatively stained ( a ) and positively stained ( b ) for CSLEX1; this tumor showed both membrane and cytoplasmic brown staining. A tumor with negative ( c ) and positive cytoplasmic brown staining ( d ) for VEGF-C; similar faint cytoplasmic brown staining as shown in negatively stained tumors for VEGF-C was seen in phosphate buffered saline controles for the VEGF-C staining; this background staining could be clearly differentiated from positive cytoplasmic brown staining for VEGF-C. A tumor with negative ( e ) and positive cytoplasmic brown staining ( f ) for VEGF-D; a brown stromal background staining was seen

Techniques Used: Expressing, Staining

19) Product Images from "Dynamics of bone healing after osteotomy with piezosurgery or conventional drilling - histomorphometrical, immunohistochemical, and molecular analysis"

Article Title: Dynamics of bone healing after osteotomy with piezosurgery or conventional drilling - histomorphometrical, immunohistochemical, and molecular analysis

Journal: Journal of Translational Medicine

doi: 10.1186/1479-5876-11-221

Immunolabeling of early healing and bone remodeling markers. Left: Immunolabeling of Vascular endothelial growth factor (VEGF) and Caspase-3 (CAS-3) of tissue sections obtained at 3, 7, and 14 days after drilling (Drill) or piezosuregry (Piezo). Right: Immunolabeling of Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) of tissue sections obtained at 7 and 14 days after drilling (Drill) or piezosuregry (Piezo). Sections were stained with the chromogen substrate diaminobenzidine and counterstained with hematoxylin. Staining scores were categorized as negative, positive (brown-yellow color), superpositive (brown color), and hyperpositive (intense brown color) (see Methods). Left (VEGF and CAS-3): at 3 days, only a few posivite regions in brown-yellow color are observed in both groups. Hyperpositive immunolabeling (intense brown color) is visible only at 7 days. At 14 days, the expression of VEGF and CAS-3 tended to be positive (brown-yellow) and superpositive (brown color). Right (OPG, RANKL and OC): at 7 days, hyperpositive immunostaining (intense brown color) is observed for OPG and OC, whereas superpositive immunoreaction (brown color) was detected for RANKL. At 14 days postsurgery, superpositive labeling (brown color) is observed for all three markers. In the negative controls no immunopositivity was detected at all times.
Figure Legend Snippet: Immunolabeling of early healing and bone remodeling markers. Left: Immunolabeling of Vascular endothelial growth factor (VEGF) and Caspase-3 (CAS-3) of tissue sections obtained at 3, 7, and 14 days after drilling (Drill) or piezosuregry (Piezo). Right: Immunolabeling of Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) of tissue sections obtained at 7 and 14 days after drilling (Drill) or piezosuregry (Piezo). Sections were stained with the chromogen substrate diaminobenzidine and counterstained with hematoxylin. Staining scores were categorized as negative, positive (brown-yellow color), superpositive (brown color), and hyperpositive (intense brown color) (see Methods). Left (VEGF and CAS-3): at 3 days, only a few posivite regions in brown-yellow color are observed in both groups. Hyperpositive immunolabeling (intense brown color) is visible only at 7 days. At 14 days, the expression of VEGF and CAS-3 tended to be positive (brown-yellow) and superpositive (brown color). Right (OPG, RANKL and OC): at 7 days, hyperpositive immunostaining (intense brown color) is observed for OPG and OC, whereas superpositive immunoreaction (brown color) was detected for RANKL. At 14 days postsurgery, superpositive labeling (brown color) is observed for all three markers. In the negative controls no immunopositivity was detected at all times.

Techniques Used: Immunolabeling, Staining, Expressing, Immunostaining, Labeling

Immonohistochemical analysis of bone remodeling markers during the bone regeneration process. Percentile ranks of immunolabeling for Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) at 7 and 14 days after surgery, in bone defects generated by drilling (Drill) or piezosuregry (Piezo). No statistically significant differences were found across all time points (n = 3).
Figure Legend Snippet: Immonohistochemical analysis of bone remodeling markers during the bone regeneration process. Percentile ranks of immunolabeling for Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) at 7 and 14 days after surgery, in bone defects generated by drilling (Drill) or piezosuregry (Piezo). No statistically significant differences were found across all time points (n = 3).

Techniques Used: Immunolabeling, Generated

20) Product Images from "Versican and vascular endothelial growth factor expression levels in peritoneal metastases from colorectal cancer are associated with survival after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy"

Article Title: Versican and vascular endothelial growth factor expression levels in peritoneal metastases from colorectal cancer are associated with survival after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy

Journal: Clinical & Experimental Metastasis

doi: 10.1007/s10585-016-9779-9

Kaplan–Meier curves of all patients. The graphs depict the curves according to the dichotomised vascular endothelial growth factor (VEGF) ( a ), microvessel density (MVD) ( b ), epithelial versican (VCAN) ( c ) and stromal VCAN ( d ) categories
Figure Legend Snippet: Kaplan–Meier curves of all patients. The graphs depict the curves according to the dichotomised vascular endothelial growth factor (VEGF) ( a ), microvessel density (MVD) ( b ), epithelial versican (VCAN) ( c ) and stromal VCAN ( d ) categories

Techniques Used:

Representative examples of versican (VCAN) ( a , b , c ) and vascular endothelial growth factor (VEGF) ( d , e , f ) expression patterns and microvessel density (MVD) ( g , h , i ) in peritoneal lesions. The magnification is shown on the micrographs. Intensities were classified as negative, weak, moderate or strong. Scoring percentages of all markers are listed next. Stromal VCAN expression: negative (1.5 %), weak (28.4 %), moderate (32.8 %) and strong (37.3 %). Epithelial VCAN expression: negative (13.4 %), weak (14.9 %), moderate (26.9 %) and strong (44.8 %). VEGF expression: weak (11.9 %), moderate (43.3 %) and strong (44.8 %)
Figure Legend Snippet: Representative examples of versican (VCAN) ( a , b , c ) and vascular endothelial growth factor (VEGF) ( d , e , f ) expression patterns and microvessel density (MVD) ( g , h , i ) in peritoneal lesions. The magnification is shown on the micrographs. Intensities were classified as negative, weak, moderate or strong. Scoring percentages of all markers are listed next. Stromal VCAN expression: negative (1.5 %), weak (28.4 %), moderate (32.8 %) and strong (37.3 %). Epithelial VCAN expression: negative (13.4 %), weak (14.9 %), moderate (26.9 %) and strong (44.8 %). VEGF expression: weak (11.9 %), moderate (43.3 %) and strong (44.8 %)

Techniques Used: Expressing

21) Product Images from "Calcified Rheumatic Valve Neoangiogenesis Is Associated With Vascular Endothelial Growth Factor Expression and Osteoblast-Like Bone Formation"

Article Title: Calcified Rheumatic Valve Neoangiogenesis Is Associated With Vascular Endothelial Growth Factor Expression and Osteoblast-Like Bone Formation

Journal: Circulation

doi: 10.1161/CIRCULATIONAHA.104.473165

Identification of neoangiogenesis markers in human degenerative mitral valves. A1, α -Actin immunostain. Arrow points to actin staining myofibroblast (magnification ×40). B1, von Willebrand factor immunostain. Arrow points to endothelial layer along atrial surface of mitral valve (magnification ×40). C1, CD68 immunostain (magnification ×40). D1, VEGF immunostain. Arrow points to endothelial layer along atrial surface of mitral valve (magnification ×40).
Figure Legend Snippet: Identification of neoangiogenesis markers in human degenerative mitral valves. A1, α -Actin immunostain. Arrow points to actin staining myofibroblast (magnification ×40). B1, von Willebrand factor immunostain. Arrow points to endothelial layer along atrial surface of mitral valve (magnification ×40). C1, CD68 immunostain (magnification ×40). D1, VEGF immunostain. Arrow points to endothelial layer along atrial surface of mitral valve (magnification ×40).

Techniques Used: Staining

Identification of bone matrix markers in the human degenerative mitral valves. A1, PCNA immunostain. Arrow points to brown staining nuclei (magnification ×40). B1, Osteopontin immunostain. Arrow points to myofibroblast cells expressing osteopontin (magnification ×40). C1, Osteocalcin immunostain. Arrow points to myofibroblast cells expressing osteocalcin (magnification ×40). D1, Alizarin red stain (magnification ×40).
Figure Legend Snippet: Identification of bone matrix markers in the human degenerative mitral valves. A1, PCNA immunostain. Arrow points to brown staining nuclei (magnification ×40). B1, Osteopontin immunostain. Arrow points to myofibroblast cells expressing osteopontin (magnification ×40). C1, Osteocalcin immunostain. Arrow points to myofibroblast cells expressing osteocalcin (magnification ×40). D1, Alizarin red stain (magnification ×40).

Techniques Used: Staining, Expressing

Identification of bone matrix markers in calcified human rheumatic valves. A1, PCNA immunostain (magnification ×10). A2, Osteopontin immuno-stain. Arrow points to myofibroblast staining cells (magnification ×10). B1, Alizarin red stain (magnification ×10). B2, Alizarin red stain (magnification ×40). C1, Osteocalcin immunostain (magnification ×10). C2, Osteocalcin immunostain. Arrow points to myofibroblast staining cells (magnification ×40). D1, MicroCT 3D reconstruction of calcified rheumatic valve. D2, MicroCT 3D reconstruction of uncalcified degenerative mitral valve.
Figure Legend Snippet: Identification of bone matrix markers in calcified human rheumatic valves. A1, PCNA immunostain (magnification ×10). A2, Osteopontin immuno-stain. Arrow points to myofibroblast staining cells (magnification ×10). B1, Alizarin red stain (magnification ×10). B2, Alizarin red stain (magnification ×40). C1, Osteocalcin immunostain (magnification ×10). C2, Osteocalcin immunostain. Arrow points to myofibroblast staining cells (magnification ×40). D1, MicroCT 3D reconstruction of calcified rheumatic valve. D2, MicroCT 3D reconstruction of uncalcified degenerative mitral valve.

Techniques Used: Immunostaining, Staining

22) Product Images from "HIF-1? and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia"

Article Title: HIF-1? and VEGF expression correlates with thrombus remodeling in cases of intravascular papillary endothelial hyperplasia

Journal: International Journal of Clinical and Experimental Pathology

doi:

Thrombosis area; (A) Degenerating red blood cells and aggregated platelets embedded in a fibrin mesh (H E, 400 x magnification). (B) extracellular CD31 staining in the loose fibrin meshwork (400 x magnification). (C) A few cells stained with an anti-CD68 antibody (400 x magnification). (D, E) A few cells positive for (D) MCT and (E) HIF-1α (400 x magnification). (F) VEGF was expressed in most mononuclear cells (400 x magnification).
Figure Legend Snippet: Thrombosis area; (A) Degenerating red blood cells and aggregated platelets embedded in a fibrin mesh (H E, 400 x magnification). (B) extracellular CD31 staining in the loose fibrin meshwork (400 x magnification). (C) A few cells stained with an anti-CD68 antibody (400 x magnification). (D, E) A few cells positive for (D) MCT and (E) HIF-1α (400 x magnification). (F) VEGF was expressed in most mononuclear cells (400 x magnification).

Techniques Used: Staining

IPEH area; A: Numerous papillae with cellular cores containing mononuclear and endothelial cells (blue arrowhead) and acellular hyalinized cores (red arrow) covered with a flattened endothelium (H E, 400 x magnification). B: Flattened endothelial cells covering the papillae were positive for CD31. Development of an impending acellular papilla from the cellular papilla was also observed (400 x magnification, in the green circle). C, D: Both CD68 and MCT were expressed in a few cells within the core of the cellular papillae but not in the acellular core (400 x magnification). E, F: HIF-1α and VEGF were highly expressed within the cellular core but were absent in the acellular core (400 x magnification).
Figure Legend Snippet: IPEH area; A: Numerous papillae with cellular cores containing mononuclear and endothelial cells (blue arrowhead) and acellular hyalinized cores (red arrow) covered with a flattened endothelium (H E, 400 x magnification). B: Flattened endothelial cells covering the papillae were positive for CD31. Development of an impending acellular papilla from the cellular papilla was also observed (400 x magnification, in the green circle). C, D: Both CD68 and MCT were expressed in a few cells within the core of the cellular papillae but not in the acellular core (400 x magnification). E, F: HIF-1α and VEGF were highly expressed within the cellular core but were absent in the acellular core (400 x magnification).

Techniques Used:

Organizing area; A: Many inflammatory cells infiltrated the perivascular area (H E, 400 x magnification). B: Endothelial cells forming vascular structure were positive for CD31 (400 x magnification). C: Several CD68-positive cells were observed (400 x magnification). D: A few cells positive for MCT, many of which showed degranulation (400 x magnification). E, F: Both HIF-1α and VEGF were highly expressed. HIF-1α was expressed in the majority of mononuclear cells but not in the endothelial cells. On the other hand, VEGF was expressed in both the mononuclear and endothelial cells (400 x magnification).
Figure Legend Snippet: Organizing area; A: Many inflammatory cells infiltrated the perivascular area (H E, 400 x magnification). B: Endothelial cells forming vascular structure were positive for CD31 (400 x magnification). C: Several CD68-positive cells were observed (400 x magnification). D: A few cells positive for MCT, many of which showed degranulation (400 x magnification). E, F: Both HIF-1α and VEGF were highly expressed. HIF-1α was expressed in the majority of mononuclear cells but not in the endothelial cells. On the other hand, VEGF was expressed in both the mononuclear and endothelial cells (400 x magnification).

Techniques Used:

23) Product Images from "Prognostic Roles of Cross-Talk between Peritumoral Hepatocytes and Stromal Cells in Hepatocellular Carcinoma Involving Peritumoral VEGF-C, VEGFR-1 and VEGFR-3"

Article Title: Prognostic Roles of Cross-Talk between Peritumoral Hepatocytes and Stromal Cells in Hepatocellular Carcinoma Involving Peritumoral VEGF-C, VEGFR-1 and VEGFR-3

Journal: PLoS ONE

doi: 10.1371/journal.pone.0064598

Peritumoral and intratumoral expression of VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3. Peritumoral expression of VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3 was much higher than expression of these factors in tumor tissue. ( A: VEGF-A; B: VEGFR-1; C: VEGFR-2; D: VEGF-C; E: VEGFR-3; 200×; stromal cells are indicated by arrows in E ).Black bars, 50um).
Figure Legend Snippet: Peritumoral and intratumoral expression of VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3. Peritumoral expression of VEGF-A, VEGF-C, VEGFR-1, VEGFR-2, and VEGFR-3 was much higher than expression of these factors in tumor tissue. ( A: VEGF-A; B: VEGFR-1; C: VEGFR-2; D: VEGF-C; E: VEGFR-3; 200×; stromal cells are indicated by arrows in E ).Black bars, 50um).

Techniques Used: Expressing

24) Product Images from "Nimbolide upregulates RECK by targeting miR-21 and HIF-1α in cell lines and in a hamster oral carcinogenesis model"

Article Title: Nimbolide upregulates RECK by targeting miR-21 and HIF-1α in cell lines and in a hamster oral carcinogenesis model

Journal: Scientific Reports

doi: 10.1038/s41598-017-01960-5

Nimbolide activates RECK by targeting HIF-1α and miR-21. ( A ) Immunoblot analyses of RECK, MMP-2, MMP-9 and ADAM-10 in control, empty plasmid and RECK plasmid transfected SCC4 and EAhy926 cells under normoxic and hypoxic conditions (N = 3). ( B ) Immunoblot analyses of RECK, MMP-2, VEGF and ADAM-10 in control, Control siRNA and RECK siRNA transfected cells in the absence or presence of nimbolide (1 µm). ( C ) Immunoblotting was performed to analyse the expression of HIF-1α, RECK, MMP-2 and ADAM-10 in empty vector and HIF-1α RNAi transfected cells under normoxic and hypoxic conditions in the presence or absence of nimbolide (1 µm). ( D ) Transcript expression level of miR-21 in control, empty plasmid and miR-21 plasmid in the presence or absence of nimbolide (1 µm) in SCC4 and EAhy926 cells as determined by quantitative RT-PCR. ♣ p
Figure Legend Snippet: Nimbolide activates RECK by targeting HIF-1α and miR-21. ( A ) Immunoblot analyses of RECK, MMP-2, MMP-9 and ADAM-10 in control, empty plasmid and RECK plasmid transfected SCC4 and EAhy926 cells under normoxic and hypoxic conditions (N = 3). ( B ) Immunoblot analyses of RECK, MMP-2, VEGF and ADAM-10 in control, Control siRNA and RECK siRNA transfected cells in the absence or presence of nimbolide (1 µm). ( C ) Immunoblotting was performed to analyse the expression of HIF-1α, RECK, MMP-2 and ADAM-10 in empty vector and HIF-1α RNAi transfected cells under normoxic and hypoxic conditions in the presence or absence of nimbolide (1 µm). ( D ) Transcript expression level of miR-21 in control, empty plasmid and miR-21 plasmid in the presence or absence of nimbolide (1 µm) in SCC4 and EAhy926 cells as determined by quantitative RT-PCR. ♣ p

Techniques Used: Plasmid Preparation, Transfection, Expressing, Quantitative RT-PCR

Schematic representation of the mechanism of action of nimbolide. Dietary administration of nimbolide activates RECK and prevents ECM degradation, and blocks activation of Notch signalling and HIF-1α mediated VEGF signalling thereby inhibiting angiogenesis. Nimbolide also inhibits miR-21, a negative regulator of RECK. Nimbolide prevents cancer progression by modulating the expression of genes and pathways involved in invasion and angiogenesis as well as by targeting miR-21.
Figure Legend Snippet: Schematic representation of the mechanism of action of nimbolide. Dietary administration of nimbolide activates RECK and prevents ECM degradation, and blocks activation of Notch signalling and HIF-1α mediated VEGF signalling thereby inhibiting angiogenesis. Nimbolide also inhibits miR-21, a negative regulator of RECK. Nimbolide prevents cancer progression by modulating the expression of genes and pathways involved in invasion and angiogenesis as well as by targeting miR-21.

Techniques Used: Activation Assay, Expressing

RECK downregulation activates VEGF signalling. ( A ) Transcript expression level of HIF-1α, VEGF and VEGFR2 determined by quantitative RT-PCR (N = 3). ♣ p
Figure Legend Snippet: RECK downregulation activates VEGF signalling. ( A ) Transcript expression level of HIF-1α, VEGF and VEGFR2 determined by quantitative RT-PCR (N = 3). ♣ p

Techniques Used: Expressing, Quantitative RT-PCR

Nimbolide activates RECK and inhibits pro-invasive and pro-angiogenic molecules in a cellular context. ( A ) IC 50 value for nimbolide in SCC131, SCC4 and EAhy926 cells (Alamar Blue assay). ( B ) Transcript expression level of VEGF, VEGFR2, and miR-21 by quantitative RT-PCR in SCC131, SCC4 and EAhy926 cell lines. Data are the mean ± SD of three independent experiments (N = 3). ♣ p
Figure Legend Snippet: Nimbolide activates RECK and inhibits pro-invasive and pro-angiogenic molecules in a cellular context. ( A ) IC 50 value for nimbolide in SCC131, SCC4 and EAhy926 cells (Alamar Blue assay). ( B ) Transcript expression level of VEGF, VEGFR2, and miR-21 by quantitative RT-PCR in SCC131, SCC4 and EAhy926 cell lines. Data are the mean ± SD of three independent experiments (N = 3). ♣ p

Techniques Used: Alamar Blue Assay, Expressing, Quantitative RT-PCR

25) Product Images from "Mechanism of endothelial progenitor cell recruitment into neo-vessels in adjacent non-tumor tissues in hepatocellular carcinoma"

Article Title: Mechanism of endothelial progenitor cell recruitment into neo-vessels in adjacent non-tumor tissues in hepatocellular carcinoma

Journal: BMC Cancer

doi: 10.1186/1471-2407-10-435

Immunohistochemical staining of MMP-9, TIMP-1, TIMP-2, endostatin, COX-2, and NOS-2 in tissues . Representative sections showing immunohistochemical staining of MMP-9 (A, B, and C), TIMP-1 (D, E, and F), TIMP-2 (G, H, and I), endostatin (J, K, and L), COX-2 (M, N, and O), and NOS-2 (P, Q, and R) in healthy controls (A, D, G, J, M, and P), adjacent non-tumor tissues (B, E, H, K, N, and Q) and tumor tissues (C, F, I, L, O, and R). The signals were detected by DAB staining.
Figure Legend Snippet: Immunohistochemical staining of MMP-9, TIMP-1, TIMP-2, endostatin, COX-2, and NOS-2 in tissues . Representative sections showing immunohistochemical staining of MMP-9 (A, B, and C), TIMP-1 (D, E, and F), TIMP-2 (G, H, and I), endostatin (J, K, and L), COX-2 (M, N, and O), and NOS-2 (P, Q, and R) in healthy controls (A, D, G, J, M, and P), adjacent non-tumor tissues (B, E, H, K, N, and Q) and tumor tissues (C, F, I, L, O, and R). The signals were detected by DAB staining.

Techniques Used: Immunohistochemistry, Staining

26) Product Images from "Characterization of tumor infiltrating Natural Killer cell subset"

Article Title: Characterization of tumor infiltrating Natural Killer cell subset

Journal: Oncotarget

doi:

CD56 bright CD16 dim natural killers cells are highly enriched within pleural and peritoneal fluids from cancer patients Mononuclear cells isolated either from pleural fluids collected from melanoma (A ; n = 3) and breast cancer patients (B ; n = 4), or from peritoneal fluids collected from gastric cancer (C ; n = 1) and pancreatic cancer ( D ; n = 1) patients. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown.
Figure Legend Snippet: CD56 bright CD16 dim natural killers cells are highly enriched within pleural and peritoneal fluids from cancer patients Mononuclear cells isolated either from pleural fluids collected from melanoma (A ; n = 3) and breast cancer patients (B ; n = 4), or from peritoneal fluids collected from gastric cancer (C ; n = 1) and pancreatic cancer ( D ; n = 1) patients. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown.

Techniques Used: Isolation, Expressing

Subset analysis of NK cells in Tumor infiltrating lymphocytes (TILS) Tumor samples were cultured in medium supplemented with recombinant human IL-2 for 2–3 weeks and then the tumor infiltrating lymphocytes were isolated by ficoll gradient centrifugation. NK subset analysis was performed by direct anti-CD3, CD16 and CD56 staining and flow cytometric analysis. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown. Representative samples of NK subsets distribution in breast carcinoma (A) , Melanoma (B) and colon cancer (C) , are shown. The tumor NK subset distribution is compared to that seen in decidual lymphocytes (D) and PBMC (E) as well as IL-2 treated PBMC (F) , used as control.
Figure Legend Snippet: Subset analysis of NK cells in Tumor infiltrating lymphocytes (TILS) Tumor samples were cultured in medium supplemented with recombinant human IL-2 for 2–3 weeks and then the tumor infiltrating lymphocytes were isolated by ficoll gradient centrifugation. NK subset analysis was performed by direct anti-CD3, CD16 and CD56 staining and flow cytometric analysis. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown. Representative samples of NK subsets distribution in breast carcinoma (A) , Melanoma (B) and colon cancer (C) , are shown. The tumor NK subset distribution is compared to that seen in decidual lymphocytes (D) and PBMC (E) as well as IL-2 treated PBMC (F) , used as control.

Techniques Used: Cell Culture, Recombinant, Isolation, Gradient Centrifugation, Staining, Flow Cytometry, Expressing

CD56 bright natural killer cells express specific dNK surface markers Tumor and decidual infiltrating lymphocytes were isolated as described in Figure 2 . The expression of CD56 versus either CD9 (A) or CXCR3 (B) in CD3 − -gated cells isolated from either breast tumor (A, left; n = 3), colon cancer (B, left; n = 3) or deciduas (A and B, right; n = 3), is shown. As control for IL-2 treatment, the expression of CD9 in CD3 − - CD56 high gated cells from either PBMC (black line) or IL-2 treated PBMC (grey line), is shown (C) .
Figure Legend Snippet: CD56 bright natural killer cells express specific dNK surface markers Tumor and decidual infiltrating lymphocytes were isolated as described in Figure 2 . The expression of CD56 versus either CD9 (A) or CXCR3 (B) in CD3 − -gated cells isolated from either breast tumor (A, left; n = 3), colon cancer (B, left; n = 3) or deciduas (A and B, right; n = 3), is shown. As control for IL-2 treatment, the expression of CD9 in CD3 − - CD56 high gated cells from either PBMC (black line) or IL-2 treated PBMC (grey line), is shown (C) .

Techniques Used: Isolation, Expressing

CD56 bright CD16 dim natural killers subset are highly enriched within melanoma, breast and colon tumors Lymphocytes were isolated from tumor tissues by mechanical dissociation and enzymatic digestion and were then immunostained, as above. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown. Representative samples demonstrating the enrichment of CD56 bright CD16 dim NK subset in breast (A) , colon (B) but not in Non-small cell lung carcinoma (C ; n = 4) tissues. The mean frequencies of CD56 bright CD16 dim cells out of total NK cell numbers in lymphocytes isolated either mechanically (D) or by IL-2 culturing (E) from various tumors. In comparison the percentage of CD56 bright CD16 dim cells in PBMC (D) or IL-2-treated PBMC (E), is shown. (P), PBMC; (C), colon; (Br) breast; and (Mel) Melanoma tumors. ** p
Figure Legend Snippet: CD56 bright CD16 dim natural killers subset are highly enriched within melanoma, breast and colon tumors Lymphocytes were isolated from tumor tissues by mechanical dissociation and enzymatic digestion and were then immunostained, as above. CD16 versus CD56 expression of CD3 − -gated lymphocytes is shown. Representative samples demonstrating the enrichment of CD56 bright CD16 dim NK subset in breast (A) , colon (B) but not in Non-small cell lung carcinoma (C ; n = 4) tissues. The mean frequencies of CD56 bright CD16 dim cells out of total NK cell numbers in lymphocytes isolated either mechanically (D) or by IL-2 culturing (E) from various tumors. In comparison the percentage of CD56 bright CD16 dim cells in PBMC (D) or IL-2-treated PBMC (E), is shown. (P), PBMC; (C), colon; (Br) breast; and (Mel) Melanoma tumors. ** p

Techniques Used: Isolation, Expressing

Tumor infiltrating NK cells express VEGF Confocal microscopy of representative double immunofluorescence staining for CD56 (red) and VEGF (green) expression in decidua (A) , colon tumor (B) and breast tumor (C) tissues (original magnification x600). Blue: nuclear staining using DAPI.
Figure Legend Snippet: Tumor infiltrating NK cells express VEGF Confocal microscopy of representative double immunofluorescence staining for CD56 (red) and VEGF (green) expression in decidua (A) , colon tumor (B) and breast tumor (C) tissues (original magnification x600). Blue: nuclear staining using DAPI.

Techniques Used: Confocal Microscopy, Double Immunofluorescence Staining, Expressing, Staining

Enrichment of infiltrating CD56+ natural killer (NK) cells in colon and breast tumors Immunohistochemistry staining for CD56 in breast and colon cancer samples and their adjacent normal tissues. (A) Normal breast tissue adjacent to the tumor (magnification x400); (B, C) Breast tumor tissues demonstrating infiltrating CD56 + NK cells (arrows; magnification x200 and x1000, respectively). (D) Normal colon tissue adjacent to the tumor (magnification x400); and (E, F) colon tumor tissues sections demonstrating infiltrating CD56 + NK cells (arrows; magnification x400 x1000, respectively).
Figure Legend Snippet: Enrichment of infiltrating CD56+ natural killer (NK) cells in colon and breast tumors Immunohistochemistry staining for CD56 in breast and colon cancer samples and their adjacent normal tissues. (A) Normal breast tissue adjacent to the tumor (magnification x400); (B, C) Breast tumor tissues demonstrating infiltrating CD56 + NK cells (arrows; magnification x200 and x1000, respectively). (D) Normal colon tissue adjacent to the tumor (magnification x400); and (E, F) colon tumor tissues sections demonstrating infiltrating CD56 + NK cells (arrows; magnification x400 x1000, respectively).

Techniques Used: Immunohistochemistry, Staining

27) Product Images from "Intravitreal injection of aflibercept, an anti-VEGF antagonist, down-regulates plasma von Willebrand factor in patients with age-related macular degeneration"

Article Title: Intravitreal injection of aflibercept, an anti-VEGF antagonist, down-regulates plasma von Willebrand factor in patients with age-related macular degeneration

Journal: Scientific Reports

doi: 10.1038/s41598-018-19473-0

Plasma levels of VWF antigen, ADAMTS13 activity, and VEGF-A before and after intravitreal injection of aflibercept in patients with exudative AMD. ( A ) Plasma levels of VEGF-A were significantly decreased at 1 day after injection (***p
Figure Legend Snippet: Plasma levels of VWF antigen, ADAMTS13 activity, and VEGF-A before and after intravitreal injection of aflibercept in patients with exudative AMD. ( A ) Plasma levels of VEGF-A were significantly decreased at 1 day after injection (***p

Techniques Used: Activity Assay, Injection

Plasma levels of VEGF-A, VWF antigen, and ADAMTS13 activity in patients with untreated exudative AMD and controls. ( A ) Plasma levels of VEGF-A in patients with AMD were significantly lower than those in controls (** p
Figure Legend Snippet: Plasma levels of VEGF-A, VWF antigen, and ADAMTS13 activity in patients with untreated exudative AMD and controls. ( A ) Plasma levels of VEGF-A in patients with AMD were significantly lower than those in controls (** p

Techniques Used: Activity Assay

28) Product Images from "Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC"

Article Title: Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC

Journal: BMC Cancer

doi: 10.1186/s12885-018-4044-z

CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue
Figure Legend Snippet: CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue

Techniques Used: Immunohistochemistry, Staining, Incubation, Concentration Assay

29) Product Images from "Hypoxia-inducible factor 1 alpha and vascular endothelial growth factor overexpression in ischemic colitis"

Article Title: Hypoxia-inducible factor 1 alpha and vascular endothelial growth factor overexpression in ischemic colitis

Journal: World Journal of Gastroenterology : WJG

doi: 10.3748/wjg.v11.i10.1535

Immunostaining of HIF-1 alpha or VEGF in the colon tissues. Weak HIF-1 alpha or VEGF immunoreactive cells were scattered in epithelial cells and interstitial cells in normal colon tissue (A: HIF-1 alpha; B: VEGF). In contrast, strong HIF-1 alpha or VEGF immunoreactive cells were diffusely seen in the epithelial and intestinal cells, including inflammatory cells in the ischemic colitis lesions (C: HIF-1 alpha; D: VEGF). Scale bars represent 100 μm.
Figure Legend Snippet: Immunostaining of HIF-1 alpha or VEGF in the colon tissues. Weak HIF-1 alpha or VEGF immunoreactive cells were scattered in epithelial cells and interstitial cells in normal colon tissue (A: HIF-1 alpha; B: VEGF). In contrast, strong HIF-1 alpha or VEGF immunoreactive cells were diffusely seen in the epithelial and intestinal cells, including inflammatory cells in the ischemic colitis lesions (C: HIF-1 alpha; D: VEGF). Scale bars represent 100 μm.

Techniques Used: Immunostaining

HIF-1 alpha and VEGF RNA expression levels in the colon tissues in the active and healing phases of ischemic colitis.
Figure Legend Snippet: HIF-1 alpha and VEGF RNA expression levels in the colon tissues in the active and healing phases of ischemic colitis.

Techniques Used: RNA Expression

RT-PCR analysis of HIF-1 alpha (lane 1: negative control; lane 2: rectal mucosa) and VEGF (lane 3: negative control; lane 4: rectal mucosa).
Figure Legend Snippet: RT-PCR analysis of HIF-1 alpha (lane 1: negative control; lane 2: rectal mucosa) and VEGF (lane 3: negative control; lane 4: rectal mucosa).

Techniques Used: Reverse Transcription Polymerase Chain Reaction, Negative Control

30) Product Images from "Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis"

Article Title: Synaptonemal complex protein 3 is associated with lymphangiogenesis in non-small cell lung cancer patients with lymph node metastasis

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-017-1241-5

Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm
Figure Legend Snippet: Representative immunohistochemical images of SCP3, VEGF-A, VEGF-B, VEGF-C and VEGF-D in formalin-fixed, paraffin-embedded non-small cell lung cancer (NSCLC) tissues. Scale bar = 100 μm

Techniques Used: Immunohistochemistry, Formalin-fixed Paraffin-Embedded

Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )
Figure Legend Snippet: Association between SCP3 and VEGFs in human non-small cell lung cancer (NSCLC). Correlation between SCP3, N factor (pN1 and pN2–3), and VEGF-A ( a ), VEGF-B ( b ), VEGF-C ( c ) or VEGF-D ( d )

Techniques Used:

31) Product Images from "Environmental Enrichment Protects the Retina from Early Diabetic Damage in Adult Rats"

Article Title: Environmental Enrichment Protects the Retina from Early Diabetic Damage in Adult Rats

Journal: PLoS ONE

doi: 10.1371/journal.pone.0101829

Expression of BDNF in retinas after 6 weeks of diabetes onset in SE- or EE-housed animals. In animals housed in SE a decrease in BDNF immunostaining in both inner and outer retina was observed, whereas in retinas from diabetic animals housed in EE, BDNF expression was similar to control animals kept in SE or EE. Shown are photographs representative of four eyes per group. Right panel: Assessment of the BDNF(+) immunoreactivity area. In SE-housed animals, experimental diabetes induced a decrease in BDNF(+) area which was prevented in diabetic animals housed in EE. Data are the mean ± SEM (n = 5 eyes per group); **p
Figure Legend Snippet: Expression of BDNF in retinas after 6 weeks of diabetes onset in SE- or EE-housed animals. In animals housed in SE a decrease in BDNF immunostaining in both inner and outer retina was observed, whereas in retinas from diabetic animals housed in EE, BDNF expression was similar to control animals kept in SE or EE. Shown are photographs representative of four eyes per group. Right panel: Assessment of the BDNF(+) immunoreactivity area. In SE-housed animals, experimental diabetes induced a decrease in BDNF(+) area which was prevented in diabetic animals housed in EE. Data are the mean ± SEM (n = 5 eyes per group); **p

Techniques Used: Expressing, Immunostaining

Housing conditions, and protocols for retinal functional, histological and biochemical studies. Three days after vehicle or STZ injection, adult Wistar rats were housed in a standard laboratory cage (panel A) or EE cages (panel B). Panel C: Experimental groups and protocols for functional, histological and biochemical studies. ERG was weekly recorded until week 10. Vascular permeability, GFAP immunostaining, retinal TNFα and TBARS levels were analyzed in SE- or EE-housed animals that had been diabetic for 6 weeks. VEGF levels were analyzed by Western blot and immunohistochemistry at 6 or 10 weeks of diabetes. Panel D: Diabetic animals housed in SE until week 7 were switched to EE, and ERG was weekly recorded until week 10.
Figure Legend Snippet: Housing conditions, and protocols for retinal functional, histological and biochemical studies. Three days after vehicle or STZ injection, adult Wistar rats were housed in a standard laboratory cage (panel A) or EE cages (panel B). Panel C: Experimental groups and protocols for functional, histological and biochemical studies. ERG was weekly recorded until week 10. Vascular permeability, GFAP immunostaining, retinal TNFα and TBARS levels were analyzed in SE- or EE-housed animals that had been diabetic for 6 weeks. VEGF levels were analyzed by Western blot and immunohistochemistry at 6 or 10 weeks of diabetes. Panel D: Diabetic animals housed in SE until week 7 were switched to EE, and ERG was weekly recorded until week 10.

Techniques Used: Functional Assay, Injection, Permeability, Immunostaining, Western Blot, Immunohistochemistry

Retinal histology examination after 10 weeks of diabetes. Panel A: Representative photomicrographs of retinal sections from control eyes, and eyes from diabetic animals housed in SE (DBT+SE) or EE (DBT+EE). No evident alterations in retinal morphology were observed. Panel B: Immunohistochemical detection of Brn3a(+) cells in the GCL from a control eye, a diabetic eye from an animal housed in SE or EE. A strong Brn3a-immunostaining was confined to the GCL (red). Cell nuclei were counterstained with DAPI (blue). Panel C: Total retinal thickness and RGC count evaluated by Brn3a immunostaining. These parameters did not differ among retinas from control animals housed in SE (control) and retinas from diabetic animals housed in SE or EE. Scale bar: 50 µm. Data are the mean ± SEM (n = 5 eyes per group). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors.
Figure Legend Snippet: Retinal histology examination after 10 weeks of diabetes. Panel A: Representative photomicrographs of retinal sections from control eyes, and eyes from diabetic animals housed in SE (DBT+SE) or EE (DBT+EE). No evident alterations in retinal morphology were observed. Panel B: Immunohistochemical detection of Brn3a(+) cells in the GCL from a control eye, a diabetic eye from an animal housed in SE or EE. A strong Brn3a-immunostaining was confined to the GCL (red). Cell nuclei were counterstained with DAPI (blue). Panel C: Total retinal thickness and RGC count evaluated by Brn3a immunostaining. These parameters did not differ among retinas from control animals housed in SE (control) and retinas from diabetic animals housed in SE or EE. Scale bar: 50 µm. Data are the mean ± SEM (n = 5 eyes per group). GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; ONL, outer nuclear layer; OS, outer segments of photoreceptors.

Techniques Used: Immunohistochemistry, Immunostaining

32) Product Images from "Dynamics of bone healing after osteotomy with piezosurgery or conventional drilling - histomorphometrical, immunohistochemical, and molecular analysis"

Article Title: Dynamics of bone healing after osteotomy with piezosurgery or conventional drilling - histomorphometrical, immunohistochemical, and molecular analysis

Journal: Journal of Translational Medicine

doi: 10.1186/1479-5876-11-221

Immunolabeling of early healing and bone remodeling markers. Left: Immunolabeling of Vascular endothelial growth factor (VEGF) and Caspase-3 (CAS-3) of tissue sections obtained at 3, 7, and 14 days after drilling (Drill) or piezosuregry (Piezo). Right: Immunolabeling of Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) of tissue sections obtained at 7 and 14 days after drilling (Drill) or piezosuregry (Piezo). Sections were stained with the chromogen substrate diaminobenzidine and counterstained with hematoxylin. Staining scores were categorized as negative, positive (brown-yellow color), superpositive (brown color), and hyperpositive (intense brown color) (see Methods). Left (VEGF and CAS-3): at 3 days, only a few posivite regions in brown-yellow color are observed in both groups. Hyperpositive immunolabeling (intense brown color) is visible only at 7 days. At 14 days, the expression of VEGF and CAS-3 tended to be positive (brown-yellow) and superpositive (brown color). Right (OPG, RANKL and OC): at 7 days, hyperpositive immunostaining (intense brown color) is observed for OPG and OC, whereas superpositive immunoreaction (brown color) was detected for RANKL. At 14 days postsurgery, superpositive labeling (brown color) is observed for all three markers. In the negative controls no immunopositivity was detected at all times.
Figure Legend Snippet: Immunolabeling of early healing and bone remodeling markers. Left: Immunolabeling of Vascular endothelial growth factor (VEGF) and Caspase-3 (CAS-3) of tissue sections obtained at 3, 7, and 14 days after drilling (Drill) or piezosuregry (Piezo). Right: Immunolabeling of Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) of tissue sections obtained at 7 and 14 days after drilling (Drill) or piezosuregry (Piezo). Sections were stained with the chromogen substrate diaminobenzidine and counterstained with hematoxylin. Staining scores were categorized as negative, positive (brown-yellow color), superpositive (brown color), and hyperpositive (intense brown color) (see Methods). Left (VEGF and CAS-3): at 3 days, only a few posivite regions in brown-yellow color are observed in both groups. Hyperpositive immunolabeling (intense brown color) is visible only at 7 days. At 14 days, the expression of VEGF and CAS-3 tended to be positive (brown-yellow) and superpositive (brown color). Right (OPG, RANKL and OC): at 7 days, hyperpositive immunostaining (intense brown color) is observed for OPG and OC, whereas superpositive immunoreaction (brown color) was detected for RANKL. At 14 days postsurgery, superpositive labeling (brown color) is observed for all three markers. In the negative controls no immunopositivity was detected at all times.

Techniques Used: Immunolabeling, Staining, Expressing, Immunostaining, Labeling

Immonohistochemical analysis of bone remodeling markers during the bone regeneration process. Percentile ranks of immunolabeling for Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) at 7 and 14 days after surgery, in bone defects generated by drilling (Drill) or piezosuregry (Piezo). No statistically significant differences were found across all time points (n = 3).
Figure Legend Snippet: Immonohistochemical analysis of bone remodeling markers during the bone regeneration process. Percentile ranks of immunolabeling for Osteoprotegerin (OPG), Receptor activator of nuclear factor kappa-B ligand (RANKL), and Osteocalcin (OC) at 7 and 14 days after surgery, in bone defects generated by drilling (Drill) or piezosuregry (Piezo). No statistically significant differences were found across all time points (n = 3).

Techniques Used: Immunolabeling, Generated

33) Product Images from "Progression of Arteriovenous Malformation: Possible Role of Vasculogenesis"

Article Title: Progression of Arteriovenous Malformation: Possible Role of Vasculogenesis

Journal: Plastic and reconstructive surgery

doi: 10.1097/PRS.0b013e3182268afd

Microvessel density in AVMs. CD31 immunohistochemical staining shows greater vascularity in Stage III compared to Stage II lesions. * p
Figure Legend Snippet: Microvessel density in AVMs. CD31 immunohistochemical staining shows greater vascularity in Stage III compared to Stage II lesions. * p

Techniques Used: Immunohistochemistry, Staining

34) Product Images from "Progression of Arteriovenous Malformation: Possible Role of Vasculogenesis"

Article Title: Progression of Arteriovenous Malformation: Possible Role of Vasculogenesis

Journal: Plastic and reconstructive surgery

doi: 10.1097/PRS.0b013e3182268afd

Endothelial progenitor cells (EPCs) in AVMs. Immunoflourescence using CD34 (red) and CD133 (green) antibodies shows EPCs (yellow) in AVMs but not in control tissue. Stage III lesions have greater EPCs compared to Stage II lesions, suggesting that EPCs
Figure Legend Snippet: Endothelial progenitor cells (EPCs) in AVMs. Immunoflourescence using CD34 (red) and CD133 (green) antibodies shows EPCs (yellow) in AVMs but not in control tissue. Stage III lesions have greater EPCs compared to Stage II lesions, suggesting that EPCs

Techniques Used:

35) Product Images from "An investigation of the resolution of inflammation (catabasis) in COPD"

Article Title: An investigation of the resolution of inflammation (catabasis) in COPD

Journal: Respiratory Research

doi: 10.1186/1465-9921-13-101

Individual and mean (bars) values of the proportion of macrophages with intense staining for CD44 , CD36, VEGF and TGFβ in patients with COPD, smokers with normal spirometry and non-smokers. (S = current smokers; EX-S = former smokers; NS = non-smokers). For further explanations, see text.
Figure Legend Snippet: Individual and mean (bars) values of the proportion of macrophages with intense staining for CD44 , CD36, VEGF and TGFβ in patients with COPD, smokers with normal spirometry and non-smokers. (S = current smokers; EX-S = former smokers; NS = non-smokers). For further explanations, see text.

Techniques Used: Staining

Representative examples of different macrophage immunostaining intensities (absent/moderate vs. intense staining) for CD44, CD36, VEGF and TGFβ. For further explanations, see text.
Figure Legend Snippet: Representative examples of different macrophage immunostaining intensities (absent/moderate vs. intense staining) for CD44, CD36, VEGF and TGFβ. For further explanations, see text.

Techniques Used: Immunostaining, Staining

36) Product Images from "Role of inflammatory cells, cytokines and matrix metalloproteinases in neutrophil-mediated skin diseases"

Article Title: Role of inflammatory cells, cytokines and matrix metalloproteinases in neutrophil-mediated skin diseases

Journal: Clinical and Experimental Immunology

doi: 10.1111/j.1365-2249.2010.04201.x

Immunohistochemical reactivity of inflammatory cell markers (CD3, CD163 and myeloperoxidase), cytokines [tumour necrosis factor (TNF)-α, interleukin (IL)-8 and IL-17], metalloproteinases (MMP-2 and MMP-9) and vascular endothelial growth factor
Figure Legend Snippet: Immunohistochemical reactivity of inflammatory cell markers (CD3, CD163 and myeloperoxidase), cytokines [tumour necrosis factor (TNF)-α, interleukin (IL)-8 and IL-17], metalloproteinases (MMP-2 and MMP-9) and vascular endothelial growth factor

Techniques Used: Immunohistochemistry

Immunohistochemical reactivity of inflammatory cell markers (CD3, CD163 and myeloperoxidase), cytokines (TNF-α, IL-8 and IL-17), metalloproteinases (MMP-2 and MMP-9) and vascular endothelial growth factor (VEGF) in ulcerative pyoderma gangrenosum
Figure Legend Snippet: Immunohistochemical reactivity of inflammatory cell markers (CD3, CD163 and myeloperoxidase), cytokines (TNF-α, IL-8 and IL-17), metalloproteinases (MMP-2 and MMP-9) and vascular endothelial growth factor (VEGF) in ulcerative pyoderma gangrenosum

Techniques Used: Immunohistochemistry

37) Product Images from "Clinicopathological and prognostic significance of galectin-1 and vascular endothelial growth factor expression in gastric cancer"

Article Title: Clinicopathological and prognostic significance of galectin-1 and vascular endothelial growth factor expression in gastric cancer

Journal: World Journal of Gastroenterology : WJG

doi: 10.3748/wjg.v19.i13.2073

Vascular endothelial growth factor was expressed more frequently in galectin-1-positive gastric cancers than galectin-1-negative.
Figure Legend Snippet: Vascular endothelial growth factor was expressed more frequently in galectin-1-positive gastric cancers than galectin-1-negative.

Techniques Used:

Correlation between galectin-1 and VEGF expression and clinicopathological features
Figure Legend Snippet: Correlation between galectin-1 and VEGF expression and clinicopathological features

Techniques Used: Expressing

Immunohistochemical staining for galectin-1 and vascular endothelial growth factor (original magnification, × 200). A: Positive galectin-1 expression in gastric cancer tissue; B: Positive vascular endothelial growth factor expression in gastric
Figure Legend Snippet: Immunohistochemical staining for galectin-1 and vascular endothelial growth factor (original magnification, × 200). A: Positive galectin-1 expression in gastric cancer tissue; B: Positive vascular endothelial growth factor expression in gastric

Techniques Used: Immunohistochemistry, Staining, Expressing

Correlation between galectin-1 and VEGF expression and clinicopathological features
Figure Legend Snippet: Correlation between galectin-1 and VEGF expression and clinicopathological features

Techniques Used: Expressing

38) Product Images from "Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC"

Article Title: Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC

Journal: BMC Cancer

doi: 10.1186/s12885-018-4044-z

CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue
Figure Legend Snippet: CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue

Techniques Used: Immunohistochemistry, Staining, Incubation, Concentration Assay

CD8 + T cells ( a , b ), FOXP3 + Tregs (c,dD) and CD56 + NK cells (E, F) in the sections of axillary lymph nodes (ALNs), using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer pH 6 (20 mins). The sections were then incubated with MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e : low percentage of CD8 + T cells, FOXP3 + Tregs and low number of CD56 + NK cells respectively; B , d , d : high percentage of CD8 + T cells, FOXP3 + Tregs and high number of CD56 + NK cells respectively. The positively brown membrane-stained cells (CD8 + T cells) and brown nuclear-stained cells (FOXP3 + Tregs) in non-metastatic paracortical areas of ALNs were quantified as the average % of all cells (5 HPFs). CD56 + NK cells were quantified as average number of cell count per HPF in non-metastatic para-cortical areas of ALNs with the greatest accumulation of the positively brown membrane-stained cells
Figure Legend Snippet: CD8 + T cells ( a , b ), FOXP3 + Tregs (c,dD) and CD56 + NK cells (E, F) in the sections of axillary lymph nodes (ALNs), using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer pH 6 (20 mins). The sections were then incubated with MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e : low percentage of CD8 + T cells, FOXP3 + Tregs and low number of CD56 + NK cells respectively; B , d , d : high percentage of CD8 + T cells, FOXP3 + Tregs and high number of CD56 + NK cells respectively. The positively brown membrane-stained cells (CD8 + T cells) and brown nuclear-stained cells (FOXP3 + Tregs) in non-metastatic paracortical areas of ALNs were quantified as the average % of all cells (5 HPFs). CD56 + NK cells were quantified as average number of cell count per HPF in non-metastatic para-cortical areas of ALNs with the greatest accumulation of the positively brown membrane-stained cells

Techniques Used: Immunohistochemistry, Staining, Incubation, Concentration Assay, Cell Counting

39) Product Images from "Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC"

Article Title: Tumour-draining axillary lymph nodes in patients with large and locally advanced breast cancers undergoing neoadjuvant chemotherapy (NAC): the crucial contribution of immune cells (effector, regulatory) and cytokines (Th1, Th2) to immune-mediated tumour cell death induced by NAC

Journal: BMC Cancer

doi: 10.1186/s12885-018-4044-z

CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue
Figure Legend Snippet: CD4 + ( a , b ), CD8 + (C, D) T lymphocytes, FOXP3 + Tregs ( e , f ) and CD56 + NK cells ( G , H ) in the sections of metastatic tumours, using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer, pH 6 (20 mins). The sections were then incubated with MAbs to CD4 (Dako, M7310) at a 1:80 dilution for 30 mins at RT, MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e , g low level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK cell infiltration respectively; b , d , f , h : high level of CD4 + , CD8 + T cell, FOXP3 + Treg, CD56 + NK infiltration respectively. The average number of brown membrane-stained cells (CD4 + , CD8 + T cells, CD56 + NK cells) and brown nuclear-stained cells (FOXP3 + Tregs) regardless of intensity, in contact with tumour cells or within tumour cell nests per HPF was counted. MTu: Metastatic tumour nest; LN: Lymphoid tissue

Techniques Used: Immunohistochemistry, Staining, Incubation, Concentration Assay

CD8 + T cells ( a , b ), FOXP3 + Tregs (c,dD) and CD56 + NK cells (E, F) in the sections of axillary lymph nodes (ALNs), using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer pH 6 (20 mins). The sections were then incubated with MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e : low percentage of CD8 + T cells, FOXP3 + Tregs and low number of CD56 + NK cells respectively; B , d , d : high percentage of CD8 + T cells, FOXP3 + Tregs and high number of CD56 + NK cells respectively. The positively brown membrane-stained cells (CD8 + T cells) and brown nuclear-stained cells (FOXP3 + Tregs) in non-metastatic paracortical areas of ALNs were quantified as the average % of all cells (5 HPFs). CD56 + NK cells were quantified as average number of cell count per HPF in non-metastatic para-cortical areas of ALNs with the greatest accumulation of the positively brown membrane-stained cells
Figure Legend Snippet: CD8 + T cells ( a , b ), FOXP3 + Tregs (c,dD) and CD56 + NK cells (E, F) in the sections of axillary lymph nodes (ALNs), using IHC staining, at 400× magnification. Briefly, heat-mediated antigen retrieval was performed using citrate buffer pH 6 (20 mins). The sections were then incubated with MAbs to CD8 (Dako, M7103) at a 1:100 dilution for 30 mins at RT, MAbs to FOXP3 (Abcam, ab20034) at a concentration of 20 μg/ml for 30 mins at RT, MAbs to CD56 (Dako, M7304) at a 1:50 dilution for 30 mins at RT. Polymeric HRP-linker antibody conjugate was used as secondary antibody. DAB chromogen was used to visualize the staining. The sections were counterstained with haematoxylin. a , c , e : low percentage of CD8 + T cells, FOXP3 + Tregs and low number of CD56 + NK cells respectively; B , d , d : high percentage of CD8 + T cells, FOXP3 + Tregs and high number of CD56 + NK cells respectively. The positively brown membrane-stained cells (CD8 + T cells) and brown nuclear-stained cells (FOXP3 + Tregs) in non-metastatic paracortical areas of ALNs were quantified as the average % of all cells (5 HPFs). CD56 + NK cells were quantified as average number of cell count per HPF in non-metastatic para-cortical areas of ALNs with the greatest accumulation of the positively brown membrane-stained cells

Techniques Used: Immunohistochemistry, Staining, Incubation, Concentration Assay, Cell Counting

40) Product Images from "Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients"

Article Title: Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients

Journal: British Journal of Cancer

doi: 10.1038/sj.bjc.6601992

Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-A expression and VEGF-C expression in tumour cells. The survival rates of patients who had high VEGF-A and VEGF-C expression in tumour cells and patients who had low VEGF-A and VEGF-C expression in tumour cell were 45.1 and 66.6%, respectively. The survival rates of patients who had high VEGF-A and low VEGF-C expression in tumour cells and patients who had low VEGF-A and high VEGF-C expression in tumour cell were 71.6 and 59.7%, respectively.
Figure Legend Snippet: Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-A expression and VEGF-C expression in tumour cells. The survival rates of patients who had high VEGF-A and VEGF-C expression in tumour cells and patients who had low VEGF-A and VEGF-C expression in tumour cell were 45.1 and 66.6%, respectively. The survival rates of patients who had high VEGF-A and low VEGF-C expression in tumour cells and patients who had low VEGF-A and high VEGF-C expression in tumour cell were 71.6 and 59.7%, respectively.

Techniques Used: Expressing

Expression of VEGF-C in NSCLC. Vascular endothelial growth factor C was observed in ( A ) tumour cells and ( B ) stromal macrophages.
Figure Legend Snippet: Expression of VEGF-C in NSCLC. Vascular endothelial growth factor C was observed in ( A ) tumour cells and ( B ) stromal macrophages.

Techniques Used: Expressing

Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-C expression in tumour cells: patients who had high staining for VEGF-C showed significantly less favourable survival rates compared with patients who had low staining for VEGF-C ( P =0.046).
Figure Legend Snippet: Postoperative survival of completely resected p-stage I–IIIA NSCLC. Comparison according to the status of VEGF-C expression in tumour cells: patients who had high staining for VEGF-C showed significantly less favourable survival rates compared with patients who had low staining for VEGF-C ( P =0.046).

Techniques Used: Expressing, Staining

Related Articles

Immunohistochemistry:

Article Title: Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients
Article Snippet: .. Immunohistochemical staining Expression of VEGF-C was evaluated with IHS using a streptavidin–biotinylated horseradish peroxidase detection system (LSAB+kit/HRP; DAKO, Kyoto, Japan). .. After retrieval of the antigen with heating in a microwave oven for 15 min, sections were incubated overnight at 4°C with an anti-VEGF-C goat polyclonal antibody (N-19; Santa Cruz, San Diego, CA, USA) diluted at 1 : 50.

Article Title: Fibrosarcomatous changes and expression of CD34+ and apolipoprotein-D in dermatofibrosarcoma protuberans
Article Snippet: .. Immunohistochemical expression of CD34 (Qbend-10, 1-100 dilution, Dako, Carpinteria CA, USA) and Apo-D (36C6, 1-200 dilution, Novocastra, New-castle-on-Tyne, UK) were assessed by two pathologists (M-G. and L.Z.) in all patients with adequate tumor tissue. .. Detection of the two antibodies was performed on a Dako automated immunostainer with universal detection kit streptavidin biotin-alkaline phosphatase/red/detection system Dako after heat (Apo-D) and enzyme (CD34) induced antigen retrieval.

Article Title: CD47 prevents the elimination of diseased fibroblasts in scleroderma
Article Snippet: .. Primary antibodies Flow cytometry: CD3 (Biolegend, #100209, Clone 17A2), CD4 (Biolegend, #100422, Clone GK1.5), CD11b (BD, #554411, Clone M1/70), CD11c (Biolegend, #117324, Clone N418), CD25 (Biolegend #102035, Clone PC61), CD26 (Biolegend, #137805, Clone H194-112), CD31 (BD, #553373, Clone MEC 13.3), CD45 (Biolegend, #103110, Clone 30-F11), CD47 (Biolegend, #127527, Clone Miap301), CD326 (Biolegend, #118218, Clone G8.8), F4/80 (Biolegend, #123116, Clone BM8), PDL1 (Biolegend, #124312, Clone 10F.9G2), Sca1 (Biolegend, #108114), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9) Immunohistochemistry/Immunofluorescence: Adiponectin (abcam, #ab22554), CD3 (abcam, #ab5690), CD11b (Novus, #NB110-89474), CD26 (abcam, #ab28340), CD26 (R & D, #AF954), CD31 (Dako, #m0823), CD47 (FisherScientific, #14-0479-82, Clone B6H12), CD47 (R & D, #AF1866), CD68 (Agilent, #GA60691-2, Clone KP1), Cleaved Caspase 3 (CST, #96645, Clone 5A1E), FSP1 (MilliporeSigma, #07-2274), FSP1 (Abcam, #ab58597), Collagen 1 (Abcam, #ab34710), FSP1 (MilliporeSigma, #07-2274), Ki67 (abcam, #ab15580), PD1 (Cell marque, #315M-96, Clone NAT105), PD1 (R & D, #AF1021), PDL1 (R & D, #AF1019), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9). .. Western c-Jun (CST, #9165S, Clone 60A8), FSP1 (MilliporeSigma, #07-2274), GAPD (GeneTex, #627408, Clone GT239), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9), phospho Stat3 (CST, #9131S).

Flow Cytometry:

Article Title: CD47 prevents the elimination of diseased fibroblasts in scleroderma
Article Snippet: .. Primary antibodies Flow cytometry: CD3 (Biolegend, #100209, Clone 17A2), CD4 (Biolegend, #100422, Clone GK1.5), CD11b (BD, #554411, Clone M1/70), CD11c (Biolegend, #117324, Clone N418), CD25 (Biolegend #102035, Clone PC61), CD26 (Biolegend, #137805, Clone H194-112), CD31 (BD, #553373, Clone MEC 13.3), CD45 (Biolegend, #103110, Clone 30-F11), CD47 (Biolegend, #127527, Clone Miap301), CD326 (Biolegend, #118218, Clone G8.8), F4/80 (Biolegend, #123116, Clone BM8), PDL1 (Biolegend, #124312, Clone 10F.9G2), Sca1 (Biolegend, #108114), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9) Immunohistochemistry/Immunofluorescence: Adiponectin (abcam, #ab22554), CD3 (abcam, #ab5690), CD11b (Novus, #NB110-89474), CD26 (abcam, #ab28340), CD26 (R & D, #AF954), CD31 (Dako, #m0823), CD47 (FisherScientific, #14-0479-82, Clone B6H12), CD47 (R & D, #AF1866), CD68 (Agilent, #GA60691-2, Clone KP1), Cleaved Caspase 3 (CST, #96645, Clone 5A1E), FSP1 (MilliporeSigma, #07-2274), FSP1 (Abcam, #ab58597), Collagen 1 (Abcam, #ab34710), FSP1 (MilliporeSigma, #07-2274), Ki67 (abcam, #ab15580), PD1 (Cell marque, #315M-96, Clone NAT105), PD1 (R & D, #AF1021), PDL1 (R & D, #AF1019), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9). .. Western c-Jun (CST, #9165S, Clone 60A8), FSP1 (MilliporeSigma, #07-2274), GAPD (GeneTex, #627408, Clone GT239), phospho c-Jun (Ser73) (CST, #32705, Clone D47G9), phospho Stat3 (CST, #9131S).

Blocking Assay:

Article Title: Single-cell analysis reveals diverse stromal subsets associated with immune evasion in triple-negative breast cancer
Article Snippet: .. Slides were incubated with primary antibodies diluted in blocking buffer: anti-CD31 (1:50; Agilent Technologies #M0823) and anti-CD146 (1:600; Abcam #ab75769). .. Secondary antibody staining, nuclear counterstaining and microscopy were performed as described above.

Incubation:

Article Title: Single-cell analysis reveals diverse stromal subsets associated with immune evasion in triple-negative breast cancer
Article Snippet: .. Slides were incubated with primary antibodies diluted in blocking buffer: anti-CD31 (1:50; Agilent Technologies #M0823) and anti-CD146 (1:600; Abcam #ab75769). .. Secondary antibody staining, nuclear counterstaining and microscopy were performed as described above.

Expressing:

Article Title: Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients
Article Snippet: .. Immunohistochemical staining Expression of VEGF-C was evaluated with IHS using a streptavidin–biotinylated horseradish peroxidase detection system (LSAB+kit/HRP; DAKO, Kyoto, Japan). .. After retrieval of the antigen with heating in a microwave oven for 15 min, sections were incubated overnight at 4°C with an anti-VEGF-C goat polyclonal antibody (N-19; Santa Cruz, San Diego, CA, USA) diluted at 1 : 50.

Article Title: Fibrosarcomatous changes and expression of CD34+ and apolipoprotein-D in dermatofibrosarcoma protuberans
Article Snippet: .. Immunohistochemical expression of CD34 (Qbend-10, 1-100 dilution, Dako, Carpinteria CA, USA) and Apo-D (36C6, 1-200 dilution, Novocastra, New-castle-on-Tyne, UK) were assessed by two pathologists (M-G. and L.Z.) in all patients with adequate tumor tissue. .. Detection of the two antibodies was performed on a Dako automated immunostainer with universal detection kit streptavidin biotin-alkaline phosphatase/red/detection system Dako after heat (Apo-D) and enzyme (CD34) induced antigen retrieval.

Marker:

Article Title: Identification of an Effective Early Signaling Signature during Neo-Vasculogenesis In Vivo by Ex Vivo Proteomic Profiling
Article Snippet: .. Slides were exposed to un-conjugated monoclonal mouse anti-human antibodies specifically binding vimentin (human mesodermal derived cell marker which can label mesenchymal and endothelial and hematopoietic cells, clone: V9, 0.78 µg/mL, Dako), CD31 (clone: JC70A, 5.15 µg/mL, Dako), and CD90 (clone: EPR3132, Abcam, Cambridge, MA, USA) for 30–60 min at room temperature (RT). .. Negative controls were processed identically, except that the primary antibodies were replaced by isotype-matched control antibodies in the appropriate concentration (IgG1, BD).

Staining:

Article Title: Clinical significance of VEGF-C status in tumour cells and stromal macrophages in non-small cell lung cancer patients
Article Snippet: .. Immunohistochemical staining Expression of VEGF-C was evaluated with IHS using a streptavidin–biotinylated horseradish peroxidase detection system (LSAB+kit/HRP; DAKO, Kyoto, Japan). .. After retrieval of the antigen with heating in a microwave oven for 15 min, sections were incubated overnight at 4°C with an anti-VEGF-C goat polyclonal antibody (N-19; Santa Cruz, San Diego, CA, USA) diluted at 1 : 50.

Article Title: Nerve fibers in the Tumor Microenvironment are co-localized with Tertiary Lymphoid Structures
Article Snippet: .. Sections were stained with mouse or rabbit anti-human monoclonal antibodies against CD20 (Dako, L26, 1:200), CD21 (DAKO, 1:25, CD23 (Leica, CD23-1B12, 1:50), CD4 (DAKO, 4B12 1:50), CD8 (DAKO, C8/144B, 1:50), FOXP3 (DAKO, PCH101, 1:50). .. All sections were cover slipped using Vectashield Hardset 1500 mounting medium with DAPI and slides were scanned and digitalized using the Roche Ventana scanner.

Binding Assay:

Article Title: Identification of an Effective Early Signaling Signature during Neo-Vasculogenesis In Vivo by Ex Vivo Proteomic Profiling
Article Snippet: .. Slides were exposed to un-conjugated monoclonal mouse anti-human antibodies specifically binding vimentin (human mesodermal derived cell marker which can label mesenchymal and endothelial and hematopoietic cells, clone: V9, 0.78 µg/mL, Dako), CD31 (clone: JC70A, 5.15 µg/mL, Dako), and CD90 (clone: EPR3132, Abcam, Cambridge, MA, USA) for 30–60 min at room temperature (RT). .. Negative controls were processed identically, except that the primary antibodies were replaced by isotype-matched control antibodies in the appropriate concentration (IgG1, BD).

Derivative Assay:

Article Title: Identification of an Effective Early Signaling Signature during Neo-Vasculogenesis In Vivo by Ex Vivo Proteomic Profiling
Article Snippet: .. Slides were exposed to un-conjugated monoclonal mouse anti-human antibodies specifically binding vimentin (human mesodermal derived cell marker which can label mesenchymal and endothelial and hematopoietic cells, clone: V9, 0.78 µg/mL, Dako), CD31 (clone: JC70A, 5.15 µg/mL, Dako), and CD90 (clone: EPR3132, Abcam, Cambridge, MA, USA) for 30–60 min at room temperature (RT). .. Negative controls were processed identically, except that the primary antibodies were replaced by isotype-matched control antibodies in the appropriate concentration (IgG1, BD).

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  • 88
    Agilent technologies vegf promoter
    <t>VEGF</t> is a direct <t>WT1</t> target gene. A , a schematic diagram of the VEGF promoter-luciferase reporter construct showing four putative WT1 binding sites, the HRE, and the dual internal ribosome entry site ( IRES ), and transcriptional start sites. Trans start , transcriptional start site; Alt trans start , alternate transcriptional start site. B , NIH3T3 cells were transfected with the VEGF promoter-luciferase reporter construct and either the empty pCB6 expression vector or pCB6 containing the cDNA for the indicated WT1 isoform. Relative luciferase activity is indicated on the y axis . The ** indicates values that are statistically significantly different from control with p
    Vegf Promoter, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 88/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Agilent technologies mutant vegf promoter reporters
    <t>VEGF</t> is a direct <t>WT1</t> target gene. A , a schematic diagram of the VEGF promoter-luciferase reporter construct showing four putative WT1 binding sites, the HRE, and the dual internal ribosome entry site ( IRES ), and transcriptional start sites. Trans start , transcriptional start site; Alt trans start , alternate transcriptional start site. B , NIH3T3 cells were transfected with the VEGF promoter-luciferase reporter construct and either the empty pCB6 expression vector or pCB6 containing the cDNA for the indicated WT1 isoform. Relative luciferase activity is indicated on the y axis . The ** indicates values that are statistically significantly different from control with p
    Mutant Vegf Promoter Reporters, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Agilent technologies 752 tata mut vegf luc
    <t>VEGF</t> is a direct <t>WT1</t> target gene. A , a schematic diagram of the VEGF promoter-luciferase reporter construct showing four putative WT1 binding sites, the HRE, and the dual internal ribosome entry site ( IRES ), and transcriptional start sites. Trans start , transcriptional start site; Alt trans start , alternate transcriptional start site. B , NIH3T3 cells were transfected with the VEGF promoter-luciferase reporter construct and either the empty pCB6 expression vector or pCB6 containing the cDNA for the indicated WT1 isoform. Relative luciferase activity is indicated on the y axis . The ** indicates values that are statistically significantly different from control with p
    752 Tata Mut Vegf Luc, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    VEGF is a direct WT1 target gene. A , a schematic diagram of the VEGF promoter-luciferase reporter construct showing four putative WT1 binding sites, the HRE, and the dual internal ribosome entry site ( IRES ), and transcriptional start sites. Trans start , transcriptional start site; Alt trans start , alternate transcriptional start site. B , NIH3T3 cells were transfected with the VEGF promoter-luciferase reporter construct and either the empty pCB6 expression vector or pCB6 containing the cDNA for the indicated WT1 isoform. Relative luciferase activity is indicated on the y axis . The ** indicates values that are statistically significantly different from control with p

    Journal: The Journal of Biological Chemistry

    Article Title: WT1 Protein Directly Regulates Expression of Vascular Endothelial Growth Factor and Is a Mediator of Tumor Response to Hypoxia *

    doi: 10.1074/jbc.M111.310128

    Figure Lengend Snippet: VEGF is a direct WT1 target gene. A , a schematic diagram of the VEGF promoter-luciferase reporter construct showing four putative WT1 binding sites, the HRE, and the dual internal ribosome entry site ( IRES ), and transcriptional start sites. Trans start , transcriptional start site; Alt trans start , alternate transcriptional start site. B , NIH3T3 cells were transfected with the VEGF promoter-luciferase reporter construct and either the empty pCB6 expression vector or pCB6 containing the cDNA for the indicated WT1 isoform. Relative luciferase activity is indicated on the y axis . The ** indicates values that are statistically significantly different from control with p

    Article Snippet: Mutations in putative WT1 binding sites in the VEGF promoter were prepared using the QuikChange site-directed mutagenesis kit (Agilent Technologies, Santa Clara, CA) on the luciferase reporter plasmid pPVEGF-luc.

    Techniques: Luciferase, Construct, Binding Assay, Transfection, Expressing, Plasmid Preparation, Activity Assay

    WT1 and VEGF levels correlate. A , RNA was isolated from the indicated cell lines and analyzed by quantitative RT-PCR using WT1-specific primers designed to amplify all isoforms. The signal obtained from the WT1-null SK-ES-1 cell line was arbitrarily assigned a value of 1.0, and all other signals were compared with this using the ΔΔCt method. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , quantitative RT-PCR was used to evaluate VEGF RNA expression in the indicated cell lines. The VEGF level of SK-ES-1 was arbitrarily set at 1.0. Numbers indicate p values of the differences between each WT1-expressing cell line and SK-ES-1. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. C , relative VEGF mRNA expression (as determined by quantitative RT-PCR) was plotted against relative WT1 mRNA expression (as determined by quantitative RT-PCR). Standard linear regression analysis was performed to quantify the correlation between these values, and the coefficient of correlation was found to be R 2 = 0.826.

    Journal: The Journal of Biological Chemistry

    Article Title: WT1 Protein Directly Regulates Expression of Vascular Endothelial Growth Factor and Is a Mediator of Tumor Response to Hypoxia *

    doi: 10.1074/jbc.M111.310128

    Figure Lengend Snippet: WT1 and VEGF levels correlate. A , RNA was isolated from the indicated cell lines and analyzed by quantitative RT-PCR using WT1-specific primers designed to amplify all isoforms. The signal obtained from the WT1-null SK-ES-1 cell line was arbitrarily assigned a value of 1.0, and all other signals were compared with this using the ΔΔCt method. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , quantitative RT-PCR was used to evaluate VEGF RNA expression in the indicated cell lines. The VEGF level of SK-ES-1 was arbitrarily set at 1.0. Numbers indicate p values of the differences between each WT1-expressing cell line and SK-ES-1. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. C , relative VEGF mRNA expression (as determined by quantitative RT-PCR) was plotted against relative WT1 mRNA expression (as determined by quantitative RT-PCR). Standard linear regression analysis was performed to quantify the correlation between these values, and the coefficient of correlation was found to be R 2 = 0.826.

    Article Snippet: Mutations in putative WT1 binding sites in the VEGF promoter were prepared using the QuikChange site-directed mutagenesis kit (Agilent Technologies, Santa Clara, CA) on the luciferase reporter plasmid pPVEGF-luc.

    Techniques: Isolation, Quantitative RT-PCR, RNA Expression, Expressing

    WT1 does not stabilize HIF-1. A , chromatin was immunoprecipitated from MHH-ES cells grown under normoxia or hypoxia (1% O 2 ) as well as from SK-ES-1 cells transfected with an empty expression vector (pCB6; labeled “ Control ”) or a pCB6 expression vector containing cDNA for the indicated WT1 isoform using antibody against HIF-1α or a control IgG. DNA was recovered from the immunoprecipitated chromatin and analyzed by quantitative PCR using primers surrounding the HRE in the VEGF promoter. The graph shows the relative enrichment of HRE in the HIF-1α immunoprecipitates compared with IgG control. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , RNA was isolated from the same SK-ES-1 cells used for the experiment in A and reverse transcribed. RT-PCR was performed using primers that amplify WT1 ( top ) and the ribosomal RNA 36B4 ( bottom ). This experiment was repeated three times.

    Journal: The Journal of Biological Chemistry

    Article Title: WT1 Protein Directly Regulates Expression of Vascular Endothelial Growth Factor and Is a Mediator of Tumor Response to Hypoxia *

    doi: 10.1074/jbc.M111.310128

    Figure Lengend Snippet: WT1 does not stabilize HIF-1. A , chromatin was immunoprecipitated from MHH-ES cells grown under normoxia or hypoxia (1% O 2 ) as well as from SK-ES-1 cells transfected with an empty expression vector (pCB6; labeled “ Control ”) or a pCB6 expression vector containing cDNA for the indicated WT1 isoform using antibody against HIF-1α or a control IgG. DNA was recovered from the immunoprecipitated chromatin and analyzed by quantitative PCR using primers surrounding the HRE in the VEGF promoter. The graph shows the relative enrichment of HRE in the HIF-1α immunoprecipitates compared with IgG control. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , RNA was isolated from the same SK-ES-1 cells used for the experiment in A and reverse transcribed. RT-PCR was performed using primers that amplify WT1 ( top ) and the ribosomal RNA 36B4 ( bottom ). This experiment was repeated three times.

    Article Snippet: Mutations in putative WT1 binding sites in the VEGF promoter were prepared using the QuikChange site-directed mutagenesis kit (Agilent Technologies, Santa Clara, CA) on the luciferase reporter plasmid pPVEGF-luc.

    Techniques: Immunoprecipitation, Transfection, Expressing, Plasmid Preparation, Labeling, Real-time Polymerase Chain Reaction, Isolation, Reverse Transcription Polymerase Chain Reaction

    Inhibition of WT1 expression attenuates response to hypoxia. A , MHH-ES were cultured in 1% O 2 for 48 h, and WT1 expression was determined by quantitative RT-PCR. Hypoxia caused a 2.2-fold increase in WT1 mRNA expression ( p = 0.007). Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , schematic representation of the inducible promoter system illustrating how addition of RSL results in transcriptional activation of the WT1 shRNA. C , MHH-ES cells stably transfected with either a WT1-specific shRNA or a control scrambled RNA under the control of the RSL-inducible promoter were grown for 72 h in 1% O 2 and then treated with RSL for 48 h to induce the shRNA or control. RNA was then harvested, and WT1 and VEGF expression was quantified using quantitative RT-PCR. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. D , MHH-ES cells transfected with WT1-specific shRNA were grown under either normoxic or hypoxic (1% O 2 ) conditions for 48 h. Chromatin immunoprecipitation was then performed using either an antibody against RNA polymerase II ( PolII ) or HIF-1 ( HIF ), and then those samples and unmanipulated input ( In ) DNA were subjected to PCR with primers surrounding the HRE in the VEGF promoter. RR-1 , RheoReceptor-1; RA , RheoActivator.

    Journal: The Journal of Biological Chemistry

    Article Title: WT1 Protein Directly Regulates Expression of Vascular Endothelial Growth Factor and Is a Mediator of Tumor Response to Hypoxia *

    doi: 10.1074/jbc.M111.310128

    Figure Lengend Snippet: Inhibition of WT1 expression attenuates response to hypoxia. A , MHH-ES were cultured in 1% O 2 for 48 h, and WT1 expression was determined by quantitative RT-PCR. Hypoxia caused a 2.2-fold increase in WT1 mRNA expression ( p = 0.007). Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. B , schematic representation of the inducible promoter system illustrating how addition of RSL results in transcriptional activation of the WT1 shRNA. C , MHH-ES cells stably transfected with either a WT1-specific shRNA or a control scrambled RNA under the control of the RSL-inducible promoter were grown for 72 h in 1% O 2 and then treated with RSL for 48 h to induce the shRNA or control. RNA was then harvested, and WT1 and VEGF expression was quantified using quantitative RT-PCR. Error bars represent S.E. of experiments done in triplicate. Experiments were repeated a minimum of three times. D , MHH-ES cells transfected with WT1-specific shRNA were grown under either normoxic or hypoxic (1% O 2 ) conditions for 48 h. Chromatin immunoprecipitation was then performed using either an antibody against RNA polymerase II ( PolII ) or HIF-1 ( HIF ), and then those samples and unmanipulated input ( In ) DNA were subjected to PCR with primers surrounding the HRE in the VEGF promoter. RR-1 , RheoReceptor-1; RA , RheoActivator.

    Article Snippet: Mutations in putative WT1 binding sites in the VEGF promoter were prepared using the QuikChange site-directed mutagenesis kit (Agilent Technologies, Santa Clara, CA) on the luciferase reporter plasmid pPVEGF-luc.

    Techniques: Inhibition, Expressing, Cell Culture, Quantitative RT-PCR, Activation Assay, shRNA, Stable Transfection, Transfection, Chromatin Immunoprecipitation, Polymerase Chain Reaction

    Modulating WT1 expression in Ewing sarcoma cell lines affects VEGF expression. A , the WT1-null cell line SK-ES-1 was transiently transfected with either the empty pCB6 vector or the same vector containing cDNA for the indicated WT1 isoform. Relative VEGF mRNA expression was determined by quantitative RT-PCR. The * indicates p values

    Journal: The Journal of Biological Chemistry

    Article Title: WT1 Protein Directly Regulates Expression of Vascular Endothelial Growth Factor and Is a Mediator of Tumor Response to Hypoxia *

    doi: 10.1074/jbc.M111.310128

    Figure Lengend Snippet: Modulating WT1 expression in Ewing sarcoma cell lines affects VEGF expression. A , the WT1-null cell line SK-ES-1 was transiently transfected with either the empty pCB6 vector or the same vector containing cDNA for the indicated WT1 isoform. Relative VEGF mRNA expression was determined by quantitative RT-PCR. The * indicates p values

    Article Snippet: Mutations in putative WT1 binding sites in the VEGF promoter were prepared using the QuikChange site-directed mutagenesis kit (Agilent Technologies, Santa Clara, CA) on the luciferase reporter plasmid pPVEGF-luc.

    Techniques: Expressing, Transfection, Plasmid Preparation, Quantitative RT-PCR