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Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), <t>VEGF</t> ( f ) and <t>TNF-α</t> ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)
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1) Product Images from "Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium"

Article Title: Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium

Journal: Journal of Experimental & Clinical Cancer Research : CR

doi: 10.1186/s13046-015-0223-9

Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), VEGF ( f ) and TNF-α ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)
Figure Legend Snippet: Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), VEGF ( f ) and TNF-α ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)

Techniques Used:

Lung tumour CM and secreted-proteins enhance adhesion of A549 and SK-MES-1 cells to human brain endothelial monolayers. Confluent hCMEC/D3 cells in μ-slides were exposed to A549 CM or SK-MES-1 CM for 30 min and 24 h prior to perfusion with calcein AM stained A549 ( a ) or SK-MES-1 cells ( c ). A549 and SK-MES-1 adhesion to hCMEC/D3 cells treated with 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α at 4 and 24 h ( b ) and ( d ). Mean values from three separate experiments were statistically analysed. * p ≤ 0.05 versus control levels (100 %). e Representative images of adherent calcein-AM stained A549 [( i ) and ( ii )] and SK-MES-1 [( iii ) and ( iv )] cells to DMEM-BS [( i ) and ( iii )] and CL-treated [( ii ) and ( iv )] brain endothelial monolayers. Scale bar = 75 μm
Figure Legend Snippet: Lung tumour CM and secreted-proteins enhance adhesion of A549 and SK-MES-1 cells to human brain endothelial monolayers. Confluent hCMEC/D3 cells in μ-slides were exposed to A549 CM or SK-MES-1 CM for 30 min and 24 h prior to perfusion with calcein AM stained A549 ( a ) or SK-MES-1 cells ( c ). A549 and SK-MES-1 adhesion to hCMEC/D3 cells treated with 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α at 4 and 24 h ( b ) and ( d ). Mean values from three separate experiments were statistically analysed. * p ≤ 0.05 versus control levels (100 %). e Representative images of adherent calcein-AM stained A549 [( i ) and ( ii )] and SK-MES-1 [( iii ) and ( iv )] cells to DMEM-BS [( i ) and ( iii )] and CL-treated [( ii ) and ( iv )] brain endothelial monolayers. Scale bar = 75 μm

Techniques Used: Staining

Exposure of lung tumour CM and secreted-proteins significantly altered the brain endothelial glycocalyx. a and b Integrity of the hCMEC/D3 glycocalyx was assessed by a CBF assay following exposure of ECs for 30 min or 24 h to A549 and SKMES-1 CM ( a ), or 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α ( b ). Data from 6 independent experiments, carried out in sextuplicate, is presented as WGA-FITC fluorescence/μg protein and these values were calculated as a percentage of control. * p ≤ 0.05, ** p ≤ 0.01 vs control level. c Hyaluronan (HA) and syndecan-1 levels were measured by ELISA in hCMEC/D3 growth medium following 30 min treatment with fresh DMEM-BS (control), A549 or SK-MES-1 CM. SK-MES-1 CM vs control = p = 0.007, n = 6. nd = not detected. d and c Representative confocal images of FITC-WGA stained hCMEC/D3 cells before ( d ) and ( e ) after 30 min exposure to SKMES-1 CM. Scale bar = 40 μM
Figure Legend Snippet: Exposure of lung tumour CM and secreted-proteins significantly altered the brain endothelial glycocalyx. a and b Integrity of the hCMEC/D3 glycocalyx was assessed by a CBF assay following exposure of ECs for 30 min or 24 h to A549 and SKMES-1 CM ( a ), or 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α ( b ). Data from 6 independent experiments, carried out in sextuplicate, is presented as WGA-FITC fluorescence/μg protein and these values were calculated as a percentage of control. * p ≤ 0.05, ** p ≤ 0.01 vs control level. c Hyaluronan (HA) and syndecan-1 levels were measured by ELISA in hCMEC/D3 growth medium following 30 min treatment with fresh DMEM-BS (control), A549 or SK-MES-1 CM. SK-MES-1 CM vs control = p = 0.007, n = 6. nd = not detected. d and c Representative confocal images of FITC-WGA stained hCMEC/D3 cells before ( d ) and ( e ) after 30 min exposure to SKMES-1 CM. Scale bar = 40 μM

Techniques Used: Whole Genome Amplification, Fluorescence, Enzyme-linked Immunosorbent Assay, Staining

2) Product Images from "Vascular endothelial growth factor-C secretion is increased by advanced glycation end-products: possible implication in ocular neovascularization"

Article Title: Vascular endothelial growth factor-C secretion is increased by advanced glycation end-products: possible implication in ocular neovascularization

Journal: Molecular Vision

doi:

Reverse transcription–polymerase chain reaction (RT–PCR) analysis of VEGF-A and VEGF-C. RT–PCR analysis of VEGF-A and VEGF-C mRNA expression, respectively, in ARPE-19 A and HECV B cells cultured 24 h in standard conditions (CTR) or in the presence of AGEs (GS). GAPDH was used as the internal control. VEGF-A and VEGF-C secretion in ARPE-19 C , E: and HECV D , F: cells, respectively, after 24 h culture in CTR or in presence of AGEs (GS). The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). *p
Figure Legend Snippet: Reverse transcription–polymerase chain reaction (RT–PCR) analysis of VEGF-A and VEGF-C. RT–PCR analysis of VEGF-A and VEGF-C mRNA expression, respectively, in ARPE-19 A and HECV B cells cultured 24 h in standard conditions (CTR) or in the presence of AGEs (GS). GAPDH was used as the internal control. VEGF-A and VEGF-C secretion in ARPE-19 C , E: and HECV D , F: cells, respectively, after 24 h culture in CTR or in presence of AGEs (GS). The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). *p

Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay

Secretion of vascular endothelial growth factor (VEGF)-A and –C. VEGF-A and VEGF-C secretion in ARPE-19 ( A , C and HECV B , D cells, respectively, transfected with a scrambled siRNA sequence (siControl) or siRNA of RAGE (siRAGE) following 24 h of culture in standard conditions (CTR) or in the presence of AGEs (GS).The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). **p
Figure Legend Snippet: Secretion of vascular endothelial growth factor (VEGF)-A and –C. VEGF-A and VEGF-C secretion in ARPE-19 ( A , C and HECV B , D cells, respectively, transfected with a scrambled siRNA sequence (siControl) or siRNA of RAGE (siRAGE) following 24 h of culture in standard conditions (CTR) or in the presence of AGEs (GS).The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). **p

Techniques Used: Transfection, Sequencing, Enzyme-linked Immunosorbent Assay

3) Product Images from "Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis"

Article Title: Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis

Journal: Oncotarget

doi: 10.18632/oncotarget.8780

Effect of Nebivolol on fibrinolytic capacity, cytokines and growth factors in HOMCs and HEMCs A ., B . Expression of the fibrinolytic factors PAI and tPA by HOMCs treated or not with TGF-β and with different doses of Nebivolol (10 or 15nM) during 48 h. C . The tPA/PAI ratio as fibrinolytic capacity marker was also determined. D . and E . VEGF and IL-6 supernatant levels in HOMCs treated with TGF-β. F . TGF-β levels in transdifferentiated HEMCs supernatant. G. and H . Expression of the fibrinolytic factors PAI and tPA by HEMCs treated with different doses of Nebivolol (10 or 15nM) during 48 h. I . Levels of tPA/PAI ratio in HEMCs. The levels of these factors were measured in HOMCs and HEMCs supernatants by ELISA and results are depicted as nanograms per milligrams of total cellular proteins. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE ( n = 5). P values
Figure Legend Snippet: Effect of Nebivolol on fibrinolytic capacity, cytokines and growth factors in HOMCs and HEMCs A ., B . Expression of the fibrinolytic factors PAI and tPA by HOMCs treated or not with TGF-β and with different doses of Nebivolol (10 or 15nM) during 48 h. C . The tPA/PAI ratio as fibrinolytic capacity marker was also determined. D . and E . VEGF and IL-6 supernatant levels in HOMCs treated with TGF-β. F . TGF-β levels in transdifferentiated HEMCs supernatant. G. and H . Expression of the fibrinolytic factors PAI and tPA by HEMCs treated with different doses of Nebivolol (10 or 15nM) during 48 h. I . Levels of tPA/PAI ratio in HEMCs. The levels of these factors were measured in HOMCs and HEMCs supernatants by ELISA and results are depicted as nanograms per milligrams of total cellular proteins. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE ( n = 5). P values

Techniques Used: Expressing, Marker, Enzyme-linked Immunosorbent Assay

In vivo analysis of the alterations related to angiogenesis and the ultrafiltration capacity of the peritoneal membrane A. Immunohistochemistry staining of CD31 (vessels) and B. quantification of the total CD31 positive stained cells in the peritoneal membrane. C. Ultrafiltration capacity analysis (PET test) (30 minutes) after injecting mice with PDF in the last day of the experiment. D. Concentrations of VEGF (pg/recovered volume) measured by ELISA in the peritoneal effluents of mice. No significant (NS) differences were observed. E. - G. Kinetic curves of urea, creatinine and glucose, respectively, in the different groups of mice measured at 10, 20 and 40 minutes. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE. P values
Figure Legend Snippet: In vivo analysis of the alterations related to angiogenesis and the ultrafiltration capacity of the peritoneal membrane A. Immunohistochemistry staining of CD31 (vessels) and B. quantification of the total CD31 positive stained cells in the peritoneal membrane. C. Ultrafiltration capacity analysis (PET test) (30 minutes) after injecting mice with PDF in the last day of the experiment. D. Concentrations of VEGF (pg/recovered volume) measured by ELISA in the peritoneal effluents of mice. No significant (NS) differences were observed. E. - G. Kinetic curves of urea, creatinine and glucose, respectively, in the different groups of mice measured at 10, 20 and 40 minutes. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE. P values

Techniques Used: In Vivo, Immunohistochemistry, Staining, Positron Emission Tomography, Mouse Assay, Enzyme-linked Immunosorbent Assay

4) Product Images from "Hypoxia and TGF-? Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment"

Article Title: Hypoxia and TGF-? Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment

Journal: PLoS ONE

doi: 10.1371/journal.pone.0006896

Hypoxia and TGF-β increase VEGF and CXCR4 mRNA expression and promoter activity. (A) MDA-MB-231 cells were cultured ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h and total RNA was extracted. VEGF and CXCR4 mRNA expression (mean ± SEM) was measured by semi-quantitative RT-PCR (n = 3). * P
Figure Legend Snippet: Hypoxia and TGF-β increase VEGF and CXCR4 mRNA expression and promoter activity. (A) MDA-MB-231 cells were cultured ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h and total RNA was extracted. VEGF and CXCR4 mRNA expression (mean ± SEM) was measured by semi-quantitative RT-PCR (n = 3). * P

Techniques Used: Expressing, Activity Assay, Multiple Displacement Amplification, Cell Culture, Quantitative RT-PCR

Knockdown of HIF-1α inhibits VEGF and CXCR4 mRNA and protein expression in vitro . (A) MDA-MB-231 parental cells (P) or cells transfected with a pLKO.1 vector expressing a non-target shRNA (shNT#3 and #7) or an shRNA against HIF-1α (shHIF#3 and #11) were cultured ± 1% O 2 during 6 h. Total RNA was extracted and mean ± SEM expression of HIF-1α was measured using semi-quantitative RT-PCR (n = 3). Proteins were extracted from treated cells and HIF-1α level was assayed by Western-blotting, α-tubulin was used as loading control. * P
Figure Legend Snippet: Knockdown of HIF-1α inhibits VEGF and CXCR4 mRNA and protein expression in vitro . (A) MDA-MB-231 parental cells (P) or cells transfected with a pLKO.1 vector expressing a non-target shRNA (shNT#3 and #7) or an shRNA against HIF-1α (shHIF#3 and #11) were cultured ± 1% O 2 during 6 h. Total RNA was extracted and mean ± SEM expression of HIF-1α was measured using semi-quantitative RT-PCR (n = 3). Proteins were extracted from treated cells and HIF-1α level was assayed by Western-blotting, α-tubulin was used as loading control. * P

Techniques Used: Expressing, In Vitro, Multiple Displacement Amplification, Transfection, Plasmid Preparation, shRNA, Cell Culture, Quantitative RT-PCR, Western Blot

Hypoxia and TGF-β increase VEGF and CXCR4 transcription through proximal promoter response elements. (A) HepG2 cells were transfected with pGL3 plasmids containing full-length for 5′-deleted fragments of the human VEGF or CXCR4 promoter and the phRL-CMV plasmid. Cells were treated ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h before measuring dual-luciferase activity. Results are expressed as the mean ± SEM (n = 3) of the relative luciferase activity, analyzed using an unpaired Student's t test. (B) Schematic representation of wild-type (WT), HRE-mutant (mH1) and SBE-mutant (mS1 or mS2) VEGF and CXCR4 promoters. One to three nucleotides (underlined, bold letters) within HRE and SBEs were substituted as indicated. (C) HepG2 cells were transfected with pGL3 plasmids containing a wild-type VEGF or CXCR4 promoter or promoters with mutations to the HRE or SBE and the phRL-CMV plasmid. Cells were treated ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h before measuring dual-luciferase activity. Results are expressed as the mean ± SEM (n = 3) of the relative luciferase activity, analyzed using an unpaired Student's t test. * P
Figure Legend Snippet: Hypoxia and TGF-β increase VEGF and CXCR4 transcription through proximal promoter response elements. (A) HepG2 cells were transfected with pGL3 plasmids containing full-length for 5′-deleted fragments of the human VEGF or CXCR4 promoter and the phRL-CMV plasmid. Cells were treated ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h before measuring dual-luciferase activity. Results are expressed as the mean ± SEM (n = 3) of the relative luciferase activity, analyzed using an unpaired Student's t test. (B) Schematic representation of wild-type (WT), HRE-mutant (mH1) and SBE-mutant (mS1 or mS2) VEGF and CXCR4 promoters. One to three nucleotides (underlined, bold letters) within HRE and SBEs were substituted as indicated. (C) HepG2 cells were transfected with pGL3 plasmids containing a wild-type VEGF or CXCR4 promoter or promoters with mutations to the HRE or SBE and the phRL-CMV plasmid. Cells were treated ± TGF-β (5 ng/mL) ± 1% O 2 during 24 h before measuring dual-luciferase activity. Results are expressed as the mean ± SEM (n = 3) of the relative luciferase activity, analyzed using an unpaired Student's t test. * P

Techniques Used: Transfection, Plasmid Preparation, Luciferase, Activity Assay, Mutagenesis

HIF-1α knockdown and TGF-β blockade decreases VEGF and CXCR4 mRNA expression in vitro . (A) MDA-MB-231 dominant-negative TβRII expressing cells (DNRII) were transfected with a pLKO.1 vector expressing a non-target shRNA (DNRII/shNT#2 and #4) or an shRNA against HIF-1α (DNRII/shHIF#22 and #26) were cultured ± 1% O 2 during 6 h. Total RNA was extracted and mean ± SEM expression of HIF-1α was measured using semi-quantitative RT-PCR (n = 3). * P
Figure Legend Snippet: HIF-1α knockdown and TGF-β blockade decreases VEGF and CXCR4 mRNA expression in vitro . (A) MDA-MB-231 dominant-negative TβRII expressing cells (DNRII) were transfected with a pLKO.1 vector expressing a non-target shRNA (DNRII/shNT#2 and #4) or an shRNA against HIF-1α (DNRII/shHIF#22 and #26) were cultured ± 1% O 2 during 6 h. Total RNA was extracted and mean ± SEM expression of HIF-1α was measured using semi-quantitative RT-PCR (n = 3). * P

Techniques Used: Expressing, In Vitro, Multiple Displacement Amplification, Dominant Negative Mutation, Transfection, Plasmid Preparation, shRNA, Cell Culture, Quantitative RT-PCR

5) Product Images from "Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *"

Article Title: Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M112.392076

Short term exposure to EE produced antidepressant-like effects. A , depressive-like behaviors were measured by the TST. The immobility time during a 3-min TST was measured in mice after housing in an SE or EE for a period of 3 or 7 days. B , schematic representation of the experimental designs for examining the lasting antidepressant-like effects by EE. The antidepressant-like effects in the TST were still evident 7 days following EE treatment and were able to be restored upon re-exposure to EE. C , levels of VEGF-A proteins in the hippocampus of mice subjected to SE or EE for 7 days. D , levels of BDNF proteins in the hippocampus of mice subjected to SE or EE for 7 days. E , correlation analysis of VEGF-A levels in the hippocampus of mice and the immobility time in the TST. F , correlation analysis of BDNF levels in the hippocampus of mice and the immobility time in the TST. G , immobility time in the TST for wild type ( WT ) or heterozygous Flk-1 knock-out ( Flk-1 +/− ) mice subjected to SE or EE for 7 days. H , immobility time in the TST for homozygous BDNF-floxed or BDNF conditional knock-out (BDNF −/− ) mice subjected to SE or EE for 7 days. The total number of animals examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: Short term exposure to EE produced antidepressant-like effects. A , depressive-like behaviors were measured by the TST. The immobility time during a 3-min TST was measured in mice after housing in an SE or EE for a period of 3 or 7 days. B , schematic representation of the experimental designs for examining the lasting antidepressant-like effects by EE. The antidepressant-like effects in the TST were still evident 7 days following EE treatment and were able to be restored upon re-exposure to EE. C , levels of VEGF-A proteins in the hippocampus of mice subjected to SE or EE for 7 days. D , levels of BDNF proteins in the hippocampus of mice subjected to SE or EE for 7 days. E , correlation analysis of VEGF-A levels in the hippocampus of mice and the immobility time in the TST. F , correlation analysis of BDNF levels in the hippocampus of mice and the immobility time in the TST. G , immobility time in the TST for wild type ( WT ) or heterozygous Flk-1 knock-out ( Flk-1 +/− ) mice subjected to SE or EE for 7 days. H , immobility time in the TST for homozygous BDNF-floxed or BDNF conditional knock-out (BDNF −/− ) mice subjected to SE or EE for 7 days. The total number of animals examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Produced, Mouse Assay, Knock-Out

VEGF stimulates spinogenesis in primary cultures of mouse hippocampal neurons. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures in response to vehicle ( Veh ) or VEGF (1–100 ng/ml) treatment for 24 h. C and D , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 6–48 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: VEGF stimulates spinogenesis in primary cultures of mouse hippocampal neurons. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures in response to vehicle ( Veh ) or VEGF (1–100 ng/ml) treatment for 24 h. C and D , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 6–48 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used:

Inhibition of miR-107 increases dendritic spine number through the activation of VEGF/Flk-1 signaling. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures from WT or Flk-1 +/− mice subjected to VEGF (100 ng/ml) treatment for 24 h or transfection with antagomiR-107. Con , control; Vec , vector. C and D , representative images and summary graph showing the number of dendritic spines in antagomiR-107-transfected neuronal cultures subjected to VEGF treatment or shRNA-HIF-1α co-transfection. E , levels of VEGF-A protein secretion in hippocampal neuronal cultures from WT or Flk-1 +/− mice in response to Vec or antagomiR-107 treatments. The total number of dendrites examined or experiments performed is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: Inhibition of miR-107 increases dendritic spine number through the activation of VEGF/Flk-1 signaling. A and B , representative images and summary graph showing the number of dendritic spines in hippocampal neuronal cultures from WT or Flk-1 +/− mice subjected to VEGF (100 ng/ml) treatment for 24 h or transfection with antagomiR-107. Con , control; Vec , vector. C and D , representative images and summary graph showing the number of dendritic spines in antagomiR-107-transfected neuronal cultures subjected to VEGF treatment or shRNA-HIF-1α co-transfection. E , levels of VEGF-A protein secretion in hippocampal neuronal cultures from WT or Flk-1 +/− mice in response to Vec or antagomiR-107 treatments. The total number of dendrites examined or experiments performed is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Inhibition, Activation Assay, Mouse Assay, Transfection, Plasmid Preparation, shRNA, Cotransfection

VEGF stimulates spinogenesis through the activation of Flk-1 receptors. A and C , representative images and summary graph showing the number of dendritic spines in shRNA-DsRed- or shRNA-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. B and D , representative images and summary graph showing the number of dendritic spines in vector ( Vec )- or DN-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: VEGF stimulates spinogenesis through the activation of Flk-1 receptors. A and C , representative images and summary graph showing the number of dendritic spines in shRNA-DsRed- or shRNA-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. B and D , representative images and summary graph showing the number of dendritic spines in vector ( Vec )- or DN-Flk-1-transfected hippocampal neuronal cultures in response to VEGF (100 ng/ml) treatment for 24 h. The total number of dendrites examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Activation Assay, shRNA, Transfection, Plasmid Preparation

HIF-1α is essential for EE-induced antidepressant-like effects. A , schematic representation of the experimental designs for examining the EE-induced antidepressant-like effects in mice receiving bilateral intrahippocampal injections of shRNA-DsRed or shRNA-HIF-1α before SE or EE treatment. B , representative images showing the delivery of EGFP shRNA-HIF-1α in the CA1 region of the dorsal hippocampus. Scale, 200 μm. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in hippocampal CA1 region of mice with or without (naive) intrahippocampal injections of shRNA-DsRed or shRNA-HIF-1α and subsequently subjected to EE for 7 days. D , levels of VEGF-A proteins in the hippocampus of shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. E , immobility time in the TST for shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. F , immobility time in the TST for GFP- or CA-HIF-1α-treated mice subjected to SE or EE for 7 days. G and H , representative images and summary graph showing the number of dendritic spines of hippocampal CA1 pyramidal neurons in shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. Scale, 5 μm. The total number of animals or neurons examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: HIF-1α is essential for EE-induced antidepressant-like effects. A , schematic representation of the experimental designs for examining the EE-induced antidepressant-like effects in mice receiving bilateral intrahippocampal injections of shRNA-DsRed or shRNA-HIF-1α before SE or EE treatment. B , representative images showing the delivery of EGFP shRNA-HIF-1α in the CA1 region of the dorsal hippocampus. Scale, 200 μm. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in hippocampal CA1 region of mice with or without (naive) intrahippocampal injections of shRNA-DsRed or shRNA-HIF-1α and subsequently subjected to EE for 7 days. D , levels of VEGF-A proteins in the hippocampus of shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. E , immobility time in the TST for shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. F , immobility time in the TST for GFP- or CA-HIF-1α-treated mice subjected to SE or EE for 7 days. G and H , representative images and summary graph showing the number of dendritic spines of hippocampal CA1 pyramidal neurons in shRNA-DsRed- or shRNA-HIF-1α-treated mice subjected to SE or EE for 7 days. Scale, 5 μm. The total number of animals or neurons examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Mouse Assay, shRNA, Western Blot, Expressing

Role of miR-107 in EE-induced antidepressant-like effects. A , schematic representation of the experimental designs for examining the EE-induced antidepressant-like effects in mice receiving bilateral hippocampal overexpression ( OE ) of miR-107 before SE or EE treatment. B , representative image showing the delivery of EGFP miR-107 in the CA1 region of the dorsal hippocampus. Scale bar , 200 μm. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in hippocampal CA1 region of mice with hippocampal overexpression of vector ( Vec ) or miR-107 and subsequently subjected to EE for 7 days. D , levels of VEGF-A proteins in the hippocampus of vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. E , immobility time in the TST for vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. F and G , representative images and summary graph showing the number of dendritic spines of hippocampal CA1 pyramidal neurons in vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. Scale bar, 5 μm. The total number of animals or neurons examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: Role of miR-107 in EE-induced antidepressant-like effects. A , schematic representation of the experimental designs for examining the EE-induced antidepressant-like effects in mice receiving bilateral hippocampal overexpression ( OE ) of miR-107 before SE or EE treatment. B , representative image showing the delivery of EGFP miR-107 in the CA1 region of the dorsal hippocampus. Scale bar , 200 μm. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in hippocampal CA1 region of mice with hippocampal overexpression of vector ( Vec ) or miR-107 and subsequently subjected to EE for 7 days. D , levels of VEGF-A proteins in the hippocampus of vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. E , immobility time in the TST for vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. F and G , representative images and summary graph showing the number of dendritic spines of hippocampal CA1 pyramidal neurons in vector- or miR-107-overexpressing mice subjected to SE or EE for 7 days. Scale bar, 5 μm. The total number of animals or neurons examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Mouse Assay, Over Expression, Western Blot, Expressing, Plasmid Preparation

EE stimulates VEGF production by an up-regulation of HIF-1α . A , time course of EE-induced VEGF-A secretion in the hippocampus. B , time course of EE-induced VEGF-A mRNA expression in the hippocampus. The samples in A and B were collected from the same mice. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in the hippocampus of mice subjected to SE or EE for 1–14 days. D , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in the CA1, CA3, and dentate gyrus ( DG ) areas of the hippocampus of mice subjected to SE or EE for 3 days. The total number of animals examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p
Figure Legend Snippet: EE stimulates VEGF production by an up-regulation of HIF-1α . A , time course of EE-induced VEGF-A secretion in the hippocampus. B , time course of EE-induced VEGF-A mRNA expression in the hippocampus. The samples in A and B were collected from the same mice. C , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in the hippocampus of mice subjected to SE or EE for 1–14 days. D , representative immunoblots and corresponding densitometric analysis showing HIF-1α protein expression in the CA1, CA3, and dentate gyrus ( DG ) areas of the hippocampus of mice subjected to SE or EE for 3 days. The total number of animals examined is indicated by n in parentheses . Data are presented as means ± S.E. *, p

Techniques Used: Expressing, Mouse Assay, Western Blot

6) Product Images from "Low oxygen tension positively influences cardiomyocyte progenitor cell function"

Article Title: Low oxygen tension positively influences cardiomyocyte progenitor cell function

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/j.1582-4934.2011.01270.x

Hypoxia influences secretion of factors by hCMPCs. To determine the secretion of proteins, medium was conditioned by culturing cells for 6 or 9 days under hypoxia or normoxia. To measure protein levels, ELISA was performed. Hypoxia decreased the secretion of MCP-1 (A), TGF-β (B) and IL-8 (C). The secretion of VEGF-A (D) was induced by hypoxia, whereas PDGF-BB secretion remained unaffected (E). PlGF secretion was increased during prolonged normoxic culture and remained unaffected by hypoxia (F). Average of five experiments is shown. *Significant difference between normoxia and hypoxia at the same time-point.
Figure Legend Snippet: Hypoxia influences secretion of factors by hCMPCs. To determine the secretion of proteins, medium was conditioned by culturing cells for 6 or 9 days under hypoxia or normoxia. To measure protein levels, ELISA was performed. Hypoxia decreased the secretion of MCP-1 (A), TGF-β (B) and IL-8 (C). The secretion of VEGF-A (D) was induced by hypoxia, whereas PDGF-BB secretion remained unaffected (E). PlGF secretion was increased during prolonged normoxic culture and remained unaffected by hypoxia (F). Average of five experiments is shown. *Significant difference between normoxia and hypoxia at the same time-point.

Techniques Used: Enzyme-linked Immunosorbent Assay

7) Product Images from "von Willebrand factor fibers promote cancer-associated platelet aggregation in malignant melanoma of mice and humans"

Article Title: von Willebrand factor fibers promote cancer-associated platelet aggregation in malignant melanoma of mice and humans

Journal: Blood

doi: 10.1182/blood-2014-08-595686

Blocking VEGF-A using tinzaparin reduces VWF fiber formation in tumor microvasculature. Immunofluorescence stainings for VWF (green) and anti-CD31 (red) in cryosections of ret transgenic tumors were performed. Nuclei were stained with DAPI. Tumor microvessels of control mice showed formation of ULVWF fibers in the vessel lumen (A, arrows). By contrast, microvessels of tinzaparin-treated mice showed almost no ULVWF fiber formation and a punctual pattern of VWF within the vessel wall (B, arrowheads), indicative of reduced endothelial cell activation. Representative pictures of tumor microvessels are shown (n = 10 animals of 2 independent experiments; scale bars = 20 µm). Tinzaparin treatment correlated with a significant reduction of vessels with intraluminal VWF fibers (C). Tumor vessels were analyzed for platelet aggregation using VWF (green) and GPIb (red) staining. Quantification showed a significant increase in platelet-covered area in the lumen of tumor vessels compared with control. This effect was abolished by treatment with tinzaparin (D-E). Panel Ei shows a single platelet in the lumen of a tumor blood vessel. In addition, the treatment of ret transgenic mice with tinzaparin (gray) reduced the appearance of middle (ii) and big aggregates (iii) to healthy control skin levels (white) compared with vehicle-treated control tumors (black). Plot shows mean ± SD (n = 5-10; * P
Figure Legend Snippet: Blocking VEGF-A using tinzaparin reduces VWF fiber formation in tumor microvasculature. Immunofluorescence stainings for VWF (green) and anti-CD31 (red) in cryosections of ret transgenic tumors were performed. Nuclei were stained with DAPI. Tumor microvessels of control mice showed formation of ULVWF fibers in the vessel lumen (A, arrows). By contrast, microvessels of tinzaparin-treated mice showed almost no ULVWF fiber formation and a punctual pattern of VWF within the vessel wall (B, arrowheads), indicative of reduced endothelial cell activation. Representative pictures of tumor microvessels are shown (n = 10 animals of 2 independent experiments; scale bars = 20 µm). Tinzaparin treatment correlated with a significant reduction of vessels with intraluminal VWF fibers (C). Tumor vessels were analyzed for platelet aggregation using VWF (green) and GPIb (red) staining. Quantification showed a significant increase in platelet-covered area in the lumen of tumor vessels compared with control. This effect was abolished by treatment with tinzaparin (D-E). Panel Ei shows a single platelet in the lumen of a tumor blood vessel. In addition, the treatment of ret transgenic mice with tinzaparin (gray) reduced the appearance of middle (ii) and big aggregates (iii) to healthy control skin levels (white) compared with vehicle-treated control tumors (black). Plot shows mean ± SD (n = 5-10; * P

Techniques Used: Blocking Assay, Immunofluorescence, Transgenic Assay, Staining, Mouse Assay, Activation Assay

Tinzaparin inhibits VEGF-A–mediated angiogenesis in primary skin tumors and impedes tumor cell metastasis. Tumor-bearing mice were treated with vehicle (A; control) or tinzaparin (B) and cryosections of primary tumors were analyzed by immunofluorescences for CD31. Morphometric quantification of the vessel density (C) demonstrates a significant difference in vessel density upon tinzaparin treatment compared with control tumors. Quantitative assessment of vessels in tinzaparin-treated tumors (D) shows that tinzaparin treatment results in a significant increase of small vessels (
Figure Legend Snippet: Tinzaparin inhibits VEGF-A–mediated angiogenesis in primary skin tumors and impedes tumor cell metastasis. Tumor-bearing mice were treated with vehicle (A; control) or tinzaparin (B) and cryosections of primary tumors were analyzed by immunofluorescences for CD31. Morphometric quantification of the vessel density (C) demonstrates a significant difference in vessel density upon tinzaparin treatment compared with control tumors. Quantitative assessment of vessels in tinzaparin-treated tumors (D) shows that tinzaparin treatment results in a significant increase of small vessels (

Techniques Used: Mouse Assay

Local inhibition of ADAMTS13 promotes VWF fiber formation in microvessels obtained from human melanoma patients. Cryosections of human malignant melanoma tissue, healthy control skin, and basal cell carcinoma were analyzed by immunofluorescence stainings for VWF and CD31 (A-C) or thrombospondin (TSP) (D-E). Nuclei were stained with DAPI. Analysis of healthy skin (A) and human basal cell carcinoma (B) as control demonstrate storage of VWF in the vessel wall (arrowheads). ULVWF fibers are detected in the lumen of the microvessels, correlating to reduced VWF within the vessel wall indicative of EC activation (C, arrows). These ULVWF fibers bind platelets (D, arrows) and are associated with microthrombi formation in distinct microvessels (E, asterisk; n = 5 to 6; scale bars = 20 µm). Quantification showed significantly increased numbers of vessels with luminal VWF fibers in tumor vasculature compared with healthy skin (F). Systemic VWF level in blood samples of malignant melanoma patients was increased compared with healthy control (G). By contrast, only a slight reduction of ADAMTS13 activity was observed (H). Tumor-derived cytokines and growth factors were measured in healthy control skin and tumor of human malignant melanoma by bio-plex. Cytokine levels of IFN-γ (I), TNF-α (J), and IL-6 (K) were increased in tumor samples compared with control skin. The concentration of VEGF-A was significantly increased within melanoma compared with control (L). Results of 9 different melanoma patients are shown (* P
Figure Legend Snippet: Local inhibition of ADAMTS13 promotes VWF fiber formation in microvessels obtained from human melanoma patients. Cryosections of human malignant melanoma tissue, healthy control skin, and basal cell carcinoma were analyzed by immunofluorescence stainings for VWF and CD31 (A-C) or thrombospondin (TSP) (D-E). Nuclei were stained with DAPI. Analysis of healthy skin (A) and human basal cell carcinoma (B) as control demonstrate storage of VWF in the vessel wall (arrowheads). ULVWF fibers are detected in the lumen of the microvessels, correlating to reduced VWF within the vessel wall indicative of EC activation (C, arrows). These ULVWF fibers bind platelets (D, arrows) and are associated with microthrombi formation in distinct microvessels (E, asterisk; n = 5 to 6; scale bars = 20 µm). Quantification showed significantly increased numbers of vessels with luminal VWF fibers in tumor vasculature compared with healthy skin (F). Systemic VWF level in blood samples of malignant melanoma patients was increased compared with healthy control (G). By contrast, only a slight reduction of ADAMTS13 activity was observed (H). Tumor-derived cytokines and growth factors were measured in healthy control skin and tumor of human malignant melanoma by bio-plex. Cytokine levels of IFN-γ (I), TNF-α (J), and IL-6 (K) were increased in tumor samples compared with control skin. The concentration of VEGF-A was significantly increased within melanoma compared with control (L). Results of 9 different melanoma patients are shown (* P

Techniques Used: Inhibition, Immunofluorescence, Staining, Activation Assay, Activity Assay, Derivative Assay, Concentration Assay

The melanoma cell line Ret induces endothelial cell stimulation via VEGF-A. HUVECs were stimulated for 15 minutes with the supernatant (sn) of the melanoma cell line Ret alone or supplemented with 0.65 mg/mL bevacizumab and thrombin (0.5 IU/mL) was used as a positive control. The efficiency of the melanoma cell-induced EC stimulation was quantified by measurement of VWF release by immunofluorescence staining (A) and by ELISA for VWF (B). Supplementation of Ret cells with bevacizumab or tinzaparin (100 IU/mL) reduced tumor cell-induced VWF release (B). Measurement of VEGF-A revealed that incubation with tinzaparin for 24 hours, 48 hours, and 72 hours resulted in a significant reduction of VEGF-A release by melanoma cells (C). The VEGF-A mRNA expression measured by real-time PCR was not affected by tinzaparin treatment of 48 hours (D). Bio-plex assays of different cell fractions showed a tinzaparin-induced reduction of VEGF-A in all fractions (E). Adding tinzaparin to Ret cell supernatant immediately before the measurements revealed an interaction of VEGF-A and tinzaparin (F). Binding of tinzaparin to VEGF-A was determined using the intrinsic tryptophan fluorescence (emission: 290 nm, excitation: 340 nm). The fluorescence of VEGF-A increases in a dose-dependent manner (G). In contrast to fondaparinux, tinzaparin exhibits a high binding affinity to VEGF-A (H). The binding of VEGF-A to tinzaparin inhibited VEGF-mediated ATP production of endothelial cells indicative for reduced cell proliferation (I). Data are presented as the mean ± SD of n = 4 of at least 2 independent experiments (* P
Figure Legend Snippet: The melanoma cell line Ret induces endothelial cell stimulation via VEGF-A. HUVECs were stimulated for 15 minutes with the supernatant (sn) of the melanoma cell line Ret alone or supplemented with 0.65 mg/mL bevacizumab and thrombin (0.5 IU/mL) was used as a positive control. The efficiency of the melanoma cell-induced EC stimulation was quantified by measurement of VWF release by immunofluorescence staining (A) and by ELISA for VWF (B). Supplementation of Ret cells with bevacizumab or tinzaparin (100 IU/mL) reduced tumor cell-induced VWF release (B). Measurement of VEGF-A revealed that incubation with tinzaparin for 24 hours, 48 hours, and 72 hours resulted in a significant reduction of VEGF-A release by melanoma cells (C). The VEGF-A mRNA expression measured by real-time PCR was not affected by tinzaparin treatment of 48 hours (D). Bio-plex assays of different cell fractions showed a tinzaparin-induced reduction of VEGF-A in all fractions (E). Adding tinzaparin to Ret cell supernatant immediately before the measurements revealed an interaction of VEGF-A and tinzaparin (F). Binding of tinzaparin to VEGF-A was determined using the intrinsic tryptophan fluorescence (emission: 290 nm, excitation: 340 nm). The fluorescence of VEGF-A increases in a dose-dependent manner (G). In contrast to fondaparinux, tinzaparin exhibits a high binding affinity to VEGF-A (H). The binding of VEGF-A to tinzaparin inhibited VEGF-mediated ATP production of endothelial cells indicative for reduced cell proliferation (I). Data are presented as the mean ± SD of n = 4 of at least 2 independent experiments (* P

Techniques Used: Cell Stimulation, Positive Control, Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Incubation, Expressing, Real-time Polymerase Chain Reaction, Binding Assay, Fluorescence

Tinzaparin attenuates proliferation of melanoma cells in primary tumor and lymph nodes and attenuates tumor progression in ret transgenic mice. Immunofluorescence stainings of tumor cell proliferation with Ki67 (green) and DAPI (nuclei, blue). Cryosections of vehicle-treated tumors (A) show more proliferating melanoma cells compared with tinzaparin-treated tumors (B; scale bars = 50 µm). Quantification showed a significant reduction of Ki67-positive cells after treatment with tinzaparin (C). Analysis of Ki67-positive tumor cells in lymph nodes of vehicle-treated ret mice and tinzaparin-treated animals was assessed by flow cytometry. Results show that tinzaparin induces a significant reduction of proliferating melanoma cells (D). Bars show mean ± SD (n = 7-10). Tumor-derived VEGF was measured in tumor and lymph nodes of ret transgenic mice (E-F) by bio-plex assay. VEGF levels were decreased in tumor samples (E) and lymph nodes (F) after treatment with tinzaparin (n = 5-7 different mice each group). Consequently, a survival benefit (G) and a reduced tumor weight (H) compared with vehicle-treated control was observed after tinzaparin treatment (n = 13 of 2 independent experiments). Plot shows mean ± SD; * P
Figure Legend Snippet: Tinzaparin attenuates proliferation of melanoma cells in primary tumor and lymph nodes and attenuates tumor progression in ret transgenic mice. Immunofluorescence stainings of tumor cell proliferation with Ki67 (green) and DAPI (nuclei, blue). Cryosections of vehicle-treated tumors (A) show more proliferating melanoma cells compared with tinzaparin-treated tumors (B; scale bars = 50 µm). Quantification showed a significant reduction of Ki67-positive cells after treatment with tinzaparin (C). Analysis of Ki67-positive tumor cells in lymph nodes of vehicle-treated ret mice and tinzaparin-treated animals was assessed by flow cytometry. Results show that tinzaparin induces a significant reduction of proliferating melanoma cells (D). Bars show mean ± SD (n = 7-10). Tumor-derived VEGF was measured in tumor and lymph nodes of ret transgenic mice (E-F) by bio-plex assay. VEGF levels were decreased in tumor samples (E) and lymph nodes (F) after treatment with tinzaparin (n = 5-7 different mice each group). Consequently, a survival benefit (G) and a reduced tumor weight (H) compared with vehicle-treated control was observed after tinzaparin treatment (n = 13 of 2 independent experiments). Plot shows mean ± SD; * P

Techniques Used: Transgenic Assay, Mouse Assay, Immunofluorescence, Flow Cytometry, Cytometry, Derivative Assay, Plex Assay

8) Product Images from "Dioxin Receptor Deficiency Impairs Angiogenesis by a Mechanism Involving VEGF-A Depletion in the Endothelium and Transforming Growth Factor-? Overexpression in the Stroma *"

Article Title: Dioxin Receptor Deficiency Impairs Angiogenesis by a Mechanism Involving VEGF-A Depletion in the Endothelium and Transforming Growth Factor-? Overexpression in the Stroma *

Journal: The Journal of Biological Chemistry

doi: 10.1074/jbc.M109.013292

AhR −/− MAECs have reduced expression and activity of the proangiogenesis factor, VEGF. A , total RNA was purified from AhR +/+ and AhR −/− MAECs and used to analyze Hif-1 α, Vegf-A , Vegf-B , Plgf , Vegfr-1 , and Vegfr-2
Figure Legend Snippet: AhR −/− MAECs have reduced expression and activity of the proangiogenesis factor, VEGF. A , total RNA was purified from AhR +/+ and AhR −/− MAECs and used to analyze Hif-1 α, Vegf-A , Vegf-B , Plgf , Vegfr-1 , and Vegfr-2

Techniques Used: Expressing, Activity Assay, Purification

Medium conditioned by AhR −/− fibroblasts inhibits invasion of HMEC-1 cells, and modulation of VEGF and TGFβ levels affects blood vessel recruitment in vivo . A , HMEC-1 cells plated in Matrigel-coated Transwells were treated with
Figure Legend Snippet: Medium conditioned by AhR −/− fibroblasts inhibits invasion of HMEC-1 cells, and modulation of VEGF and TGFβ levels affects blood vessel recruitment in vivo . A , HMEC-1 cells plated in Matrigel-coated Transwells were treated with

Techniques Used: In Vivo

AhR down-modulation by siRNA decreases Hif-1 α and Vegf-A expression in HMEC-1 cells. A , HMEC-1 cells were transfected with scramble of AhR-specific siRNA by nucleoporation. Total RNA was purified and analyzed for Hif-1 α and Vegf-A mRNA
Figure Legend Snippet: AhR down-modulation by siRNA decreases Hif-1 α and Vegf-A expression in HMEC-1 cells. A , HMEC-1 cells were transfected with scramble of AhR-specific siRNA by nucleoporation. Total RNA was purified and analyzed for Hif-1 α and Vegf-A mRNA

Techniques Used: Expressing, Transfection, Purification

VEGF activity modulates angiogenesis in an AhR-dependent manner in vivo and in culture. A , aortic rings ( ar ) were obtained from AhR +/+ and AhR −/− mice and plated in Matrigel plugs for 7 days. Sprouting of MAECs was analyzed by measuring
Figure Legend Snippet: VEGF activity modulates angiogenesis in an AhR-dependent manner in vivo and in culture. A , aortic rings ( ar ) were obtained from AhR +/+ and AhR −/− mice and plated in Matrigel plugs for 7 days. Sprouting of MAECs was analyzed by measuring

Techniques Used: Activity Assay, In Vivo, Mouse Assay

9) Product Images from "Implication of vascular endothelial growth factor A and C in revealing diagnostic lymphangiogenic markers in node-positive bladder cancer"

Article Title: Implication of vascular endothelial growth factor A and C in revealing diagnostic lymphangiogenic markers in node-positive bladder cancer

Journal: Oncotarget

doi: 10.18632/oncotarget.15669

Gene expression analysis of BCa tumor tissues as compared with normal bladder tissues A . Gene expression of 10 factors involved in tumor lymphangiogenesis in BCa tissues (T) and in normal bladder tissues obtained from the same patients (N). No significant differences were found, except for the higher expression of VEGF-A in tumor tissues than in normal tissues (Wilcoxon matched-paired test, p
Figure Legend Snippet: Gene expression analysis of BCa tumor tissues as compared with normal bladder tissues A . Gene expression of 10 factors involved in tumor lymphangiogenesis in BCa tissues (T) and in normal bladder tissues obtained from the same patients (N). No significant differences were found, except for the higher expression of VEGF-A in tumor tissues than in normal tissues (Wilcoxon matched-paired test, p

Techniques Used: Expressing, BIA-KA

SLP-76 expression and production in MEC A . The SLP-76 gene expression upon VEGF stimulation (at either concentration) and under bladder cell line trans-well assay was compared with SLP-76 gene expression elicited in anti-CD3 treated CD8 T cells (positive control). SLP-76-fold increase after direct MEC stimulation or priming with cell lines was calculated as gene expression 2-fold over its constitutive expression (arbitrary cut-off). SLP-76-fold increase in anti CD3 treated CD8 T cells was calculated as gene expression 2-fold over SLP-76 gene expression in non-stimulated CD8. Error bars represent the mean ± SD of three replicates. B . Representative fluorescent-activated cell sorting (FACS) dot plot analysis of in vitro SLP-76 intracellular staining in anti-CD3 treated CD8 T cells (upper right panel) and VEGF-C (2 ng/ml medium right panel) or VEGF-A (17 ng/ml lower right panel) stimulated CD31+ MEC, as compared with isotype staining (all left panels). Overlaid histograms refer to mean fluorescent intensity (MFI) of in vitro SLP-76 intracellular staining of CD8 T cells upon anti-CD3 induction (above) or MEC after VEGF-C (middle) or VEGF–A (below) stimulation compared with isotype staining. C . Western blot showing SLP-76 expression in MEC stimulated with either VEGF-A or VEGF-C at 50 ng/ml, over 3 and 6 h, as compared with SLP-76 expression in human CD8 T cells treated with anti-CD3 mAb (CD8 vs αCD3). D . A representative image by fluorescence microscopy (scale bar 400 μm) of MEC after 3 and 6 h of stimulation with either VEGF-A or VEGF-C (50 ng/ml). The SLP-76 basal staining (no stimulation) for both cell lines (MEC right and LEC left) is also reported. MEC were immunostained for SLP-76 (Cy-3; red), cytoskeleton (phalloidin; green), and nucleus (DAPI; blue). E . MEC migration was assessed by a scratch wound healing assay, as shown in one representative picture (scale bar 50 μm) by confocal microscopy after 24 h of VEGF-C stimulation at the standard concentration. Cells were cultured in 6-well plates and allowed to reach 80% confluence before scratching vertically and horizontally (see symbol bottom right in the upper panel). Histograms represent migration potential of cells based on the quantification of empty area (% closure rate) as compared with time 0 (100% empty area) for VEGF-A (gray bar) or VEGF-C (black bar) (p
Figure Legend Snippet: SLP-76 expression and production in MEC A . The SLP-76 gene expression upon VEGF stimulation (at either concentration) and under bladder cell line trans-well assay was compared with SLP-76 gene expression elicited in anti-CD3 treated CD8 T cells (positive control). SLP-76-fold increase after direct MEC stimulation or priming with cell lines was calculated as gene expression 2-fold over its constitutive expression (arbitrary cut-off). SLP-76-fold increase in anti CD3 treated CD8 T cells was calculated as gene expression 2-fold over SLP-76 gene expression in non-stimulated CD8. Error bars represent the mean ± SD of three replicates. B . Representative fluorescent-activated cell sorting (FACS) dot plot analysis of in vitro SLP-76 intracellular staining in anti-CD3 treated CD8 T cells (upper right panel) and VEGF-C (2 ng/ml medium right panel) or VEGF-A (17 ng/ml lower right panel) stimulated CD31+ MEC, as compared with isotype staining (all left panels). Overlaid histograms refer to mean fluorescent intensity (MFI) of in vitro SLP-76 intracellular staining of CD8 T cells upon anti-CD3 induction (above) or MEC after VEGF-C (middle) or VEGF–A (below) stimulation compared with isotype staining. C . Western blot showing SLP-76 expression in MEC stimulated with either VEGF-A or VEGF-C at 50 ng/ml, over 3 and 6 h, as compared with SLP-76 expression in human CD8 T cells treated with anti-CD3 mAb (CD8 vs αCD3). D . A representative image by fluorescence microscopy (scale bar 400 μm) of MEC after 3 and 6 h of stimulation with either VEGF-A or VEGF-C (50 ng/ml). The SLP-76 basal staining (no stimulation) for both cell lines (MEC right and LEC left) is also reported. MEC were immunostained for SLP-76 (Cy-3; red), cytoskeleton (phalloidin; green), and nucleus (DAPI; blue). E . MEC migration was assessed by a scratch wound healing assay, as shown in one representative picture (scale bar 50 μm) by confocal microscopy after 24 h of VEGF-C stimulation at the standard concentration. Cells were cultured in 6-well plates and allowed to reach 80% confluence before scratching vertically and horizontally (see symbol bottom right in the upper panel). Histograms represent migration potential of cells based on the quantification of empty area (% closure rate) as compared with time 0 (100% empty area) for VEGF-A (gray bar) or VEGF-C (black bar) (p

Techniques Used: Expressing, Concentration Assay, Positive Control, FACS, In Vitro, Staining, Western Blot, Fluorescence, Microscopy, Migration, Wound Healing Assay, Confocal Microscopy, Cell Culture

10) Product Images from "‘Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients’"

Article Title: ‘Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients’

Journal: Scientific Reports

doi: 10.1038/srep31375

Transfection with miR-124a and/or -125a mimics promoted decreased expression of inflammatory markers and their intracellular pathways. Monocytes isolated from healthy donors were transfected with 100 nmol/L miR-124a, miR-125a mimics -either separately or in conjunction-, and a non-specific control (scrambled) by using siPORT TM NeoFX TM transfection agent following manufacturer’s protocols. Forty - two hours after transfection cells were activated with 10 mg/mL LPS for 6 h, and potential targets were analyzed by qRT-PCR ( MCP-1, IL-8, IL-6, IL-6R and VEGF ), Flow cytometry (peroxides), and Western blot (STAT3, ERK, and p38MAPK). Data, obtained from 4 independent transfection experiments, were expressed as changes relative to the values of the cells transfected with scrambled control, and set as 100%. ( A,B ) Changes promoted by transfection of monocytes with miR-124a mimic. ( C,D ) Changes promoted by transfection of monocytes with miRNA mimic for miR-125a. ( E,F ) Changes promoted by simultaneous transfection of monocytes with miR-124a and miR-125a mimics. Western blots show representative results from 4 separated experiments with similar results. Lanes were run on the same gel under the same experimental conditions but were non-contiguous. Cropping lines are used in the figure. Full-length blots are presented in Supplementary Fig. S6B for key data.
Figure Legend Snippet: Transfection with miR-124a and/or -125a mimics promoted decreased expression of inflammatory markers and their intracellular pathways. Monocytes isolated from healthy donors were transfected with 100 nmol/L miR-124a, miR-125a mimics -either separately or in conjunction-, and a non-specific control (scrambled) by using siPORT TM NeoFX TM transfection agent following manufacturer’s protocols. Forty - two hours after transfection cells were activated with 10 mg/mL LPS for 6 h, and potential targets were analyzed by qRT-PCR ( MCP-1, IL-8, IL-6, IL-6R and VEGF ), Flow cytometry (peroxides), and Western blot (STAT3, ERK, and p38MAPK). Data, obtained from 4 independent transfection experiments, were expressed as changes relative to the values of the cells transfected with scrambled control, and set as 100%. ( A,B ) Changes promoted by transfection of monocytes with miR-124a mimic. ( C,D ) Changes promoted by transfection of monocytes with miRNA mimic for miR-125a. ( E,F ) Changes promoted by simultaneous transfection of monocytes with miR-124a and miR-125a mimics. Western blots show representative results from 4 separated experiments with similar results. Lanes were run on the same gel under the same experimental conditions but were non-contiguous. Cropping lines are used in the figure. Full-length blots are presented in Supplementary Fig. S6B for key data.

Techniques Used: Transfection, Expressing, Isolation, Quantitative RT-PCR, Flow Cytometry, Cytometry, Western Blot

11) Product Images from "Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis"

Article Title: Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis

Journal: Oncotarget

doi: 10.18632/oncotarget.8780

Effect of Nebivolol on fibrinolytic capacity, cytokines and growth factors in HOMCs and HEMCs A ., B . Expression of the fibrinolytic factors PAI and tPA by HOMCs treated or not with TGF-β and with different doses of Nebivolol (10 or 15nM) during 48 h. C . The tPA/PAI ratio as fibrinolytic capacity marker was also determined. D . and E . VEGF and IL-6 supernatant levels in HOMCs treated with TGF-β. F . TGF-β levels in transdifferentiated HEMCs supernatant. G. and H . Expression of the fibrinolytic factors PAI and tPA by HEMCs treated with different doses of Nebivolol (10 or 15nM) during 48 h. I . Levels of tPA/PAI ratio in HEMCs. The levels of these factors were measured in HOMCs and HEMCs supernatants by ELISA and results are depicted as nanograms per milligrams of total cellular proteins. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE ( n = 5). P values
Figure Legend Snippet: Effect of Nebivolol on fibrinolytic capacity, cytokines and growth factors in HOMCs and HEMCs A ., B . Expression of the fibrinolytic factors PAI and tPA by HOMCs treated or not with TGF-β and with different doses of Nebivolol (10 or 15nM) during 48 h. C . The tPA/PAI ratio as fibrinolytic capacity marker was also determined. D . and E . VEGF and IL-6 supernatant levels in HOMCs treated with TGF-β. F . TGF-β levels in transdifferentiated HEMCs supernatant. G. and H . Expression of the fibrinolytic factors PAI and tPA by HEMCs treated with different doses of Nebivolol (10 or 15nM) during 48 h. I . Levels of tPA/PAI ratio in HEMCs. The levels of these factors were measured in HOMCs and HEMCs supernatants by ELISA and results are depicted as nanograms per milligrams of total cellular proteins. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE ( n = 5). P values

Techniques Used: Expressing, Marker, Enzyme-linked Immunosorbent Assay

In vivo analysis of the alterations related to angiogenesis and the ultrafiltration capacity of the peritoneal membrane A. Immunohistochemistry staining of CD31 (vessels) and B. quantification of the total CD31 positive stained cells in the peritoneal membrane. C. Ultrafiltration capacity analysis (PET test) (30 minutes) after injecting mice with PDF in the last day of the experiment. D. Concentrations of VEGF (pg/recovered volume) measured by ELISA in the peritoneal effluents of mice. No significant (NS) differences were observed. E. - G. Kinetic curves of urea, creatinine and glucose, respectively, in the different groups of mice measured at 10, 20 and 40 minutes. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE. P values
Figure Legend Snippet: In vivo analysis of the alterations related to angiogenesis and the ultrafiltration capacity of the peritoneal membrane A. Immunohistochemistry staining of CD31 (vessels) and B. quantification of the total CD31 positive stained cells in the peritoneal membrane. C. Ultrafiltration capacity analysis (PET test) (30 minutes) after injecting mice with PDF in the last day of the experiment. D. Concentrations of VEGF (pg/recovered volume) measured by ELISA in the peritoneal effluents of mice. No significant (NS) differences were observed. E. - G. Kinetic curves of urea, creatinine and glucose, respectively, in the different groups of mice measured at 10, 20 and 40 minutes. Data point graphics represent the absolute value of each determination and lines the median, lower and upper range. Numbers on the top of graphics represent the mean ± SE. P values

Techniques Used: In Vivo, Immunohistochemistry, Staining, Positron Emission Tomography, Mouse Assay, Enzyme-linked Immunosorbent Assay

12) Product Images from "Rapamycin Protects from Type-I Peritoneal Membrane Failure Inhibiting the Angiogenesis, Lymphangiogenesis, and Endo-MT"

Article Title: Rapamycin Protects from Type-I Peritoneal Membrane Failure Inhibiting the Angiogenesis, Lymphangiogenesis, and Endo-MT

Journal: BioMed Research International

doi: 10.1155/2015/989560

Rapamycin decreases VEGF and TNF- α levels in the peritoneal cavity. (a) Analysis of VEGF and (b) TNF-alpha in the drained volumes shows a strong increase of these factors in PD fluid-instilled animals, and administration of Rapamycin significantly reduces their production. The one-way ANOVA test resulted in a significance of p
Figure Legend Snippet: Rapamycin decreases VEGF and TNF- α levels in the peritoneal cavity. (a) Analysis of VEGF and (b) TNF-alpha in the drained volumes shows a strong increase of these factors in PD fluid-instilled animals, and administration of Rapamycin significantly reduces their production. The one-way ANOVA test resulted in a significance of p

Techniques Used:

Rapamycin decreases the VEGF production by MCs. Omentum and PD effluent derived MCs were cultured and stimulated with Rapamycin 2 nM during 48 h. We performed two parallel cultures with equal numbers of MCs. A group received Rapamycin while the other was untreated. Supernatants were collected and VEGF-A, VEGF-C, and VEGF-D were measured. Rapamycin significantly decreased VEGFs, mainly the prolymphopenic VEGF-C and VEGF-D forms (a and b). We also calculated the reduction rate (%). Importantly in nonepithelioid MCs derived from PD effluent, VEGF-D was reduced by 82% and VEGF-C (gray bar graphic) by 63%. In omentum-derived MCs (white bar) the VEGF-D and VEGF-C were reduced by 63% and 20%, respectively (c). Box plots graphics represent 25th and 75th percentiles and median, minimum, and maximum values. Statistical differences between groups are shown (mean ± SD).
Figure Legend Snippet: Rapamycin decreases the VEGF production by MCs. Omentum and PD effluent derived MCs were cultured and stimulated with Rapamycin 2 nM during 48 h. We performed two parallel cultures with equal numbers of MCs. A group received Rapamycin while the other was untreated. Supernatants were collected and VEGF-A, VEGF-C, and VEGF-D were measured. Rapamycin significantly decreased VEGFs, mainly the prolymphopenic VEGF-C and VEGF-D forms (a and b). We also calculated the reduction rate (%). Importantly in nonepithelioid MCs derived from PD effluent, VEGF-D was reduced by 82% and VEGF-C (gray bar graphic) by 63%. In omentum-derived MCs (white bar) the VEGF-D and VEGF-C were reduced by 63% and 20%, respectively (c). Box plots graphics represent 25th and 75th percentiles and median, minimum, and maximum values. Statistical differences between groups are shown (mean ± SD).

Techniques Used: Derivative Assay, Cell Culture

Related Articles

Enzyme-linked Immunosorbent Assay:

Article Title: Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium
Article Snippet: .. Secreted levels of TNF-α, CL, CC, VEGF-A and IGFBP-7 in the A549 and SK-MES-1 CM were measured by ELISA (TNF-α and CC: Bender MedSystems, Vienna, Austria; CL: R & D systems, Abingdon, UK; VEGF-A: PeproTech®, London, UK) and IGFBP-7: in house ELISA previously described in [ ]. .. Treatment conditions During the various investigations, with the exception of E-selectin ELISA, hCMEC/D3 cells were incubated with either complete lung tumour CM (A549 CM and SK-MES-1 CM) or individual tumour secreted-proteins (at concentrations detected during the previous ELISAs) – 80 ng/ml CC (Abcam, Cambridge, UK), 10 ng/ml CL (Sigma Aldrich, Gillingham, UK), 200 ng/ml IGFBP-7 (Abcam, Cambridge, UK), 0.2 ng/ml VEGF-A (R & D Systems, Abingdon, UK) and 160 pg/ml TNF-α (Enzo Life sciences, Exeter, UK).

Article Title: Vascular endothelial growth factor-C secretion is increased by advanced glycation end-products: possible implication in ocular neovascularization
Article Snippet: .. VEGF-A and VEGF-C secretions were assessed with enzyme-linked immunosorbent assay (ELISA; Bender MedSystem, Vienna, Austria). .. VEGF-A and VEGF-C concentrations were calculated from the standards curve and normalized to the total protein concentration of the respective lysate.

Article Title: Dioxin Receptor Deficiency Impairs Angiogenesis by a Mechanism Involving VEGF-A Depletion in the Endothelium and Transforming Growth Factor-? Overexpression in the Stroma *
Article Snippet: .. The amounts of active VEGF-A, TGFβ-1, and TGFβ-2 secreted by MAECs or T-FGM fibroblasts were determined using ELISA kits from Bender MedSystems following the manufacturer's instructions. ..

Article Title: von Willebrand factor fibers promote cancer-associated platelet aggregation in malignant melanoma of mice and humans
Article Snippet: .. ELISA for VEGF-A was performed in accordance with the instructions of the manufacturer (Bender MedSystems). .. Single-cell suspension of fresh tumor tissue and lymph nodes was produced as described before.

Article Title: Low oxygen tension positively influences cardiomyocyte progenitor cell function
Article Snippet: .. ELISA We performed an ELISA for VEGF-A (Human VEGF-A ELISA, Bender MedSystems GmbH, Vienna, Austria), PlGF (PeProTech, Rocky, Hill, NJ, USA), PDGF-BB (PeProTech), monocyte chemotactic protein-1 (MCP-1; PeProTech), interleukin (IL)-8 (PeliKine Compact human IL-8 ELISA kit, Sanquin, Amsterdam, The Netherlands) and TGF-β1 (human TGF-β1 , DY240, R & D Systems, Abingdon, UK) according to the manufacturer’s protocols. ..

Article Title: Nebivolol, a β1-adrenergic blocker, protects from peritoneal membrane damage induced during peritoneal dialysis
Article Snippet: .. VEGF-A, TGF-β1 , IL-6, IL-8 and IL-10 were measured by ELISA, (VEGF-A and IL-8: Bender Med Systems, Vienna, Austria; TGF-β1 : R & D Systems, Minneapolis, USA; and IL-6 and IL-10: BD Biosciences Pharmingen, San Diego, CA). .. NO3 - was also determined in MCs supernatant and PD effluent by capillary electrophoresis as described [ ].

Article Title: Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *
Article Snippet: .. The amount of VEGF-A in hippocampal tissues or the release from cultured hippocampal neurons was measured by ELISA using a commercially available kit specific for mice VEGF-A (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions. .. The BDNF levels were measured with a conventional two-site enzyme-linked immunosorbent assay kit according to the manufacturer's protocol (Promega, Charbonnière, France).

Article Title: Hypoxia and TGF-? Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment
Article Snippet: .. VEGF enzyme-linked immunosorbant assays MDA-MB-231 parental cells and clones were plated in 12-well plates (2×105 cells/well) and grown for 48 h. After 4 h serum starvation, cells were treated ± TGF-β1 (5 ng/mL) in DMEM-FBS (1%) and ± 1% O2 for 24 h. Conditioned media was collected and analyzed by ELISA assay for VEGF-A (Bender MedSystems, Inc., Burlingame, CA), according to the manufacturer's instructions. ..

Multiple Displacement Amplification:

Article Title: Hypoxia and TGF-? Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment
Article Snippet: .. VEGF enzyme-linked immunosorbant assays MDA-MB-231 parental cells and clones were plated in 12-well plates (2×105 cells/well) and grown for 48 h. After 4 h serum starvation, cells were treated ± TGF-β1 (5 ng/mL) in DMEM-FBS (1%) and ± 1% O2 for 24 h. Conditioned media was collected and analyzed by ELISA assay for VEGF-A (Bender MedSystems, Inc., Burlingame, CA), according to the manufacturer's instructions. ..

Mouse Assay:

Article Title: Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *
Article Snippet: .. The amount of VEGF-A in hippocampal tissues or the release from cultured hippocampal neurons was measured by ELISA using a commercially available kit specific for mice VEGF-A (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions. .. The BDNF levels were measured with a conventional two-site enzyme-linked immunosorbent assay kit according to the manufacturer's protocol (Promega, Charbonnière, France).

Cell Culture:

Article Title: Vascular Endothelial Growth Factor-dependent Spinogenesis Underlies Antidepressant-like Effects of Enriched Environment *
Article Snippet: .. The amount of VEGF-A in hippocampal tissues or the release from cultured hippocampal neurons was measured by ELISA using a commercially available kit specific for mice VEGF-A (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions. .. The BDNF levels were measured with a conventional two-site enzyme-linked immunosorbent assay kit according to the manufacturer's protocol (Promega, Charbonnière, France).

Clone Assay:

Article Title: Hypoxia and TGF-? Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment
Article Snippet: .. VEGF enzyme-linked immunosorbant assays MDA-MB-231 parental cells and clones were plated in 12-well plates (2×105 cells/well) and grown for 48 h. After 4 h serum starvation, cells were treated ± TGF-β1 (5 ng/mL) in DMEM-FBS (1%) and ± 1% O2 for 24 h. Conditioned media was collected and analyzed by ELISA assay for VEGF-A (Bender MedSystems, Inc., Burlingame, CA), according to the manufacturer's instructions. ..

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    Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), <t>VEGF</t> ( f ) and <t>TNF-α</t> ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)
    Vegf A, supplied by Bender MedSystems, used in various techniques. Bioz Stars score: 92/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    <t>VEGF-C</t> and VEGF-D in M. pulmonis –infected airways. Immunohistochemical staining of VEGF-C ( A – C ) and VEGF-D ( D – F ) in mouse airways and lung 14 days after infection. ( A ) VEGF-C (green) in epithelium, peribronchial inflammatory cells,
    Vegf C, supplied by Bender MedSystems, used in various techniques. Bioz Stars score: 92/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Effect of <t>VEGF-C</t> overexpression on angiogenesis of orthotopic tumors . H E-staining of representative PC-3/VEGF-C (A, orthotopic; C, subcutaneous) tumors and PC-3/mock (B, orthotopic; D, subcutaneous) tumors. PC-3/VEGF-C tumors showed angiogenic morphology with a rich network of capillaries compared with PC-3/mock tumors. There were significantly more blood capillaries (CD34 positive, arrows) in the PC-3/VEGF-C tumors (E, 220 ± 15 μm/mm 2 , n = 29) compared with PC-3/mock tumors (F and G, 37 ± 6 μm/mm 2 , n = 24), p
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    Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), VEGF ( f ) and TNF-α ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium

    doi: 10.1186/s13046-015-0223-9

    Figure Lengend Snippet: Increased levels of E-selectin detected on the surface of human cerebral microvascular endothelial cells in response to lung tumour CM and secreted-proteins. Confluent hCMEC/D3 cells were stimulated for 4 h with A549 and SK-MES-1 CM ( a ) along with CC ( c ), CL ( d ), IGFBP-7 ( e ), VEGF ( f ) and TNF-α ( g ). E-selectin levels from 3 separate experiments, carried out in quadruplets, were statistically analysed (n ≥ 12, mean ± SD, * p ≤ 0.05 and ** p ≤ 0.01, *** p ≤ 0.005 and **** p ≤ 0.0001). Enhanced E-selectin was also detected within 30 min of CM ( a ) and secreted-proteins ( b ) exposure (* p ≤ 0.05 and ** p ≤ 0.01, n = 6)

    Article Snippet: Secreted levels of TNF-α, CL, CC, VEGF-A and IGFBP-7 in the A549 and SK-MES-1 CM were measured by ELISA (TNF-α and CC: Bender MedSystems, Vienna, Austria; CL: R & D systems, Abingdon, UK; VEGF-A: PeproTech®, London, UK) and IGFBP-7: in house ELISA previously described in [ ].

    Techniques:

    Lung tumour CM and secreted-proteins enhance adhesion of A549 and SK-MES-1 cells to human brain endothelial monolayers. Confluent hCMEC/D3 cells in μ-slides were exposed to A549 CM or SK-MES-1 CM for 30 min and 24 h prior to perfusion with calcein AM stained A549 ( a ) or SK-MES-1 cells ( c ). A549 and SK-MES-1 adhesion to hCMEC/D3 cells treated with 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α at 4 and 24 h ( b ) and ( d ). Mean values from three separate experiments were statistically analysed. * p ≤ 0.05 versus control levels (100 %). e Representative images of adherent calcein-AM stained A549 [( i ) and ( ii )] and SK-MES-1 [( iii ) and ( iv )] cells to DMEM-BS [( i ) and ( iii )] and CL-treated [( ii ) and ( iv )] brain endothelial monolayers. Scale bar = 75 μm

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium

    doi: 10.1186/s13046-015-0223-9

    Figure Lengend Snippet: Lung tumour CM and secreted-proteins enhance adhesion of A549 and SK-MES-1 cells to human brain endothelial monolayers. Confluent hCMEC/D3 cells in μ-slides were exposed to A549 CM or SK-MES-1 CM for 30 min and 24 h prior to perfusion with calcein AM stained A549 ( a ) or SK-MES-1 cells ( c ). A549 and SK-MES-1 adhesion to hCMEC/D3 cells treated with 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α at 4 and 24 h ( b ) and ( d ). Mean values from three separate experiments were statistically analysed. * p ≤ 0.05 versus control levels (100 %). e Representative images of adherent calcein-AM stained A549 [( i ) and ( ii )] and SK-MES-1 [( iii ) and ( iv )] cells to DMEM-BS [( i ) and ( iii )] and CL-treated [( ii ) and ( iv )] brain endothelial monolayers. Scale bar = 75 μm

    Article Snippet: Secreted levels of TNF-α, CL, CC, VEGF-A and IGFBP-7 in the A549 and SK-MES-1 CM were measured by ELISA (TNF-α and CC: Bender MedSystems, Vienna, Austria; CL: R & D systems, Abingdon, UK; VEGF-A: PeproTech®, London, UK) and IGFBP-7: in house ELISA previously described in [ ].

    Techniques: Staining

    Exposure of lung tumour CM and secreted-proteins significantly altered the brain endothelial glycocalyx. a and b Integrity of the hCMEC/D3 glycocalyx was assessed by a CBF assay following exposure of ECs for 30 min or 24 h to A549 and SKMES-1 CM ( a ), or 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α ( b ). Data from 6 independent experiments, carried out in sextuplicate, is presented as WGA-FITC fluorescence/μg protein and these values were calculated as a percentage of control. * p ≤ 0.05, ** p ≤ 0.01 vs control level. c Hyaluronan (HA) and syndecan-1 levels were measured by ELISA in hCMEC/D3 growth medium following 30 min treatment with fresh DMEM-BS (control), A549 or SK-MES-1 CM. SK-MES-1 CM vs control = p = 0.007, n = 6. nd = not detected. d and c Representative confocal images of FITC-WGA stained hCMEC/D3 cells before ( d ) and ( e ) after 30 min exposure to SKMES-1 CM. Scale bar = 40 μM

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium

    doi: 10.1186/s13046-015-0223-9

    Figure Lengend Snippet: Exposure of lung tumour CM and secreted-proteins significantly altered the brain endothelial glycocalyx. a and b Integrity of the hCMEC/D3 glycocalyx was assessed by a CBF assay following exposure of ECs for 30 min or 24 h to A549 and SKMES-1 CM ( a ), or 80 ng/ml CC, 10 ng/ml CL, 200 ng/ml IGFBP-7, 0.2 ng/ml VEGF and 160 pg/ml TNF-α ( b ). Data from 6 independent experiments, carried out in sextuplicate, is presented as WGA-FITC fluorescence/μg protein and these values were calculated as a percentage of control. * p ≤ 0.05, ** p ≤ 0.01 vs control level. c Hyaluronan (HA) and syndecan-1 levels were measured by ELISA in hCMEC/D3 growth medium following 30 min treatment with fresh DMEM-BS (control), A549 or SK-MES-1 CM. SK-MES-1 CM vs control = p = 0.007, n = 6. nd = not detected. d and c Representative confocal images of FITC-WGA stained hCMEC/D3 cells before ( d ) and ( e ) after 30 min exposure to SKMES-1 CM. Scale bar = 40 μM

    Article Snippet: Secreted levels of TNF-α, CL, CC, VEGF-A and IGFBP-7 in the A549 and SK-MES-1 CM were measured by ELISA (TNF-α and CC: Bender MedSystems, Vienna, Austria; CL: R & D systems, Abingdon, UK; VEGF-A: PeproTech®, London, UK) and IGFBP-7: in house ELISA previously described in [ ].

    Techniques: Whole Genome Amplification, Fluorescence, Enzyme-linked Immunosorbent Assay, Staining

    Reverse transcription–polymerase chain reaction (RT–PCR) analysis of VEGF-A and VEGF-C. RT–PCR analysis of VEGF-A and VEGF-C mRNA expression, respectively, in ARPE-19 A and HECV B cells cultured 24 h in standard conditions (CTR) or in the presence of AGEs (GS). GAPDH was used as the internal control. VEGF-A and VEGF-C secretion in ARPE-19 C , E: and HECV D , F: cells, respectively, after 24 h culture in CTR or in presence of AGEs (GS). The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). *p

    Journal: Molecular Vision

    Article Title: Vascular endothelial growth factor-C secretion is increased by advanced glycation end-products: possible implication in ocular neovascularization

    doi:

    Figure Lengend Snippet: Reverse transcription–polymerase chain reaction (RT–PCR) analysis of VEGF-A and VEGF-C. RT–PCR analysis of VEGF-A and VEGF-C mRNA expression, respectively, in ARPE-19 A and HECV B cells cultured 24 h in standard conditions (CTR) or in the presence of AGEs (GS). GAPDH was used as the internal control. VEGF-A and VEGF-C secretion in ARPE-19 C , E: and HECV D , F: cells, respectively, after 24 h culture in CTR or in presence of AGEs (GS). The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). *p

    Article Snippet: VEGF-A and VEGF-C secretions were assessed with enzyme-linked immunosorbent assay (ELISA; Bender MedSystem, Vienna, Austria).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay

    Secretion of vascular endothelial growth factor (VEGF)-A and –C. VEGF-A and VEGF-C secretion in ARPE-19 ( A , C and HECV B , D cells, respectively, transfected with a scrambled siRNA sequence (siControl) or siRNA of RAGE (siRAGE) following 24 h of culture in standard conditions (CTR) or in the presence of AGEs (GS).The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). **p

    Journal: Molecular Vision

    Article Title: Vascular endothelial growth factor-C secretion is increased by advanced glycation end-products: possible implication in ocular neovascularization

    doi:

    Figure Lengend Snippet: Secretion of vascular endothelial growth factor (VEGF)-A and –C. VEGF-A and VEGF-C secretion in ARPE-19 ( A , C and HECV B , D cells, respectively, transfected with a scrambled siRNA sequence (siControl) or siRNA of RAGE (siRAGE) following 24 h of culture in standard conditions (CTR) or in the presence of AGEs (GS).The conditioned media were collected, and ELISA was performed. Concentrations of VEGFs were calculated from standards curves and normalized to total protein. The results are representative of at least three experiments (mean±SEM). **p

    Article Snippet: VEGF-A and VEGF-C secretions were assessed with enzyme-linked immunosorbent assay (ELISA; Bender MedSystem, Vienna, Austria).

    Techniques: Transfection, Sequencing, Enzyme-linked Immunosorbent Assay

    VEGF-C and VEGF-D in M. pulmonis –infected airways. Immunohistochemical staining of VEGF-C ( A – C ) and VEGF-D ( D – F ) in mouse airways and lung 14 days after infection. ( A ) VEGF-C (green) in epithelium, peribronchial inflammatory cells,

    Journal: Journal of Clinical Investigation

    Article Title: Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation

    doi: 10.1172/JCI200522037

    Figure Lengend Snippet: VEGF-C and VEGF-D in M. pulmonis –infected airways. Immunohistochemical staining of VEGF-C ( A – C ) and VEGF-D ( D – F ) in mouse airways and lung 14 days after infection. ( A ) VEGF-C (green) in epithelium, peribronchial inflammatory cells,

    Article Snippet: VEGF-C and VEGF-D in the lungs of nude mice treated intranasally with adenoviruses encoding LacZ, VEGF165, VEGF-C, or VEGF-D ΔNΔC 10 days previously were measured by ELISA (human VEGF-C ELISA [no. BMS297; Bender MedSystems], human VEGF-D ELISA [no. DVED00; R & D Systems]).

    Techniques: Infection, Immunohistochemistry, Staining

    Effect of VEGF-C overexpression on angiogenesis of orthotopic tumors . H E-staining of representative PC-3/VEGF-C (A, orthotopic; C, subcutaneous) tumors and PC-3/mock (B, orthotopic; D, subcutaneous) tumors. PC-3/VEGF-C tumors showed angiogenic morphology with a rich network of capillaries compared with PC-3/mock tumors. There were significantly more blood capillaries (CD34 positive, arrows) in the PC-3/VEGF-C tumors (E, 220 ± 15 μm/mm 2 , n = 29) compared with PC-3/mock tumors (F and G, 37 ± 6 μm/mm 2 , n = 24), p

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Effect of VEGF-C overexpression on angiogenesis of orthotopic tumors . H E-staining of representative PC-3/VEGF-C (A, orthotopic; C, subcutaneous) tumors and PC-3/mock (B, orthotopic; D, subcutaneous) tumors. PC-3/VEGF-C tumors showed angiogenic morphology with a rich network of capillaries compared with PC-3/mock tumors. There were significantly more blood capillaries (CD34 positive, arrows) in the PC-3/VEGF-C tumors (E, 220 ± 15 μm/mm 2 , n = 29) compared with PC-3/mock tumors (F and G, 37 ± 6 μm/mm 2 , n = 24), p

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Over Expression, Staining

    Effect of VEGFR3-Ig treatment on orthotopic PC-3/VEGF-C tumors . VEGFR3-Ig fusion protein-producing construct or lacZ-Ig controls were injected intravenously into mice five minutes before orthotopic inoculation of PC-3/VEGF-C cells. The density of m-LYVE-1 positive lymphatic capillaries was decreased in VEGFR3-Ig-treated tumors (23 ± 4 μm/mm 2 , n = 8 vs . 123 ± 7 μm/mm 2 , n = 6, p

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Effect of VEGFR3-Ig treatment on orthotopic PC-3/VEGF-C tumors . VEGFR3-Ig fusion protein-producing construct or lacZ-Ig controls were injected intravenously into mice five minutes before orthotopic inoculation of PC-3/VEGF-C cells. The density of m-LYVE-1 positive lymphatic capillaries was decreased in VEGFR3-Ig-treated tumors (23 ± 4 μm/mm 2 , n = 8 vs . 123 ± 7 μm/mm 2 , n = 6, p

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Construct, Injection, Mouse Assay

    Ectopic expression of VEGF-C in PC-3 cells and orthotopic tumors . PC-3 cells were stably transfected with a vector containing human VEGF-C (PC-3/VEGF-C) or empty vector (mock). One cell clone expressing VEGF-C at a high level, and one control clone (PC-3/mock) were selected for further studies. ELISA analysis of VEGF-C protein concentration in cell lysates (A) and in conditioned media (B) revealed increased expression in PC-3/VEGF-C cells compared with PC-3/mock cells. Data are expressed as means ± SD ng/mL, corresponding 10 6 cells. (C) Western blot analysis revealed that PC-3 cell clones expressed mainly 29/31 kD form of VEGF-C. Detectable levels of 21 kD form were not seen. β-actin control was from cell lysates corresponding to the collected conditioned medium.

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Ectopic expression of VEGF-C in PC-3 cells and orthotopic tumors . PC-3 cells were stably transfected with a vector containing human VEGF-C (PC-3/VEGF-C) or empty vector (mock). One cell clone expressing VEGF-C at a high level, and one control clone (PC-3/mock) were selected for further studies. ELISA analysis of VEGF-C protein concentration in cell lysates (A) and in conditioned media (B) revealed increased expression in PC-3/VEGF-C cells compared with PC-3/mock cells. Data are expressed as means ± SD ng/mL, corresponding 10 6 cells. (C) Western blot analysis revealed that PC-3 cell clones expressed mainly 29/31 kD form of VEGF-C. Detectable levels of 21 kD form were not seen. β-actin control was from cell lysates corresponding to the collected conditioned medium.

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Expressing, Stable Transfection, Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Protein Concentration, Western Blot, Clone Assay

    Effect of VEGF-C overexpression on PC-3 prostate tumor growth . The occurrence of subcutaneous tumors of both PC-3/VEGF-C ( n = 8) and PC-3/mock ( n = 12) was 100%. (A) Subcutaneous PC-3/VEGF-C tumors grew larger (1132 ± 34 mm 3 , gray bars) than PC-3/mock tumors (47 ± 7 mm 3 , black bars) at 4 weeks and the differences in tumor volumes between the groups were significant at all time points between 2 and 4 weeks ( p

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Effect of VEGF-C overexpression on PC-3 prostate tumor growth . The occurrence of subcutaneous tumors of both PC-3/VEGF-C ( n = 8) and PC-3/mock ( n = 12) was 100%. (A) Subcutaneous PC-3/VEGF-C tumors grew larger (1132 ± 34 mm 3 , gray bars) than PC-3/mock tumors (47 ± 7 mm 3 , black bars) at 4 weeks and the differences in tumor volumes between the groups were significant at all time points between 2 and 4 weeks ( p

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Over Expression

    Effect of ectopic VEGF-C on lymphatic vessel density of orthotopic PC-3 tumors . M-LYVE-1-positive staining was observed primarily in the tumor periphery and in the peritumoral area (A-B). No differences were detected in the density of lymphatic vessels Bar 500 μm.

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Effect of ectopic VEGF-C on lymphatic vessel density of orthotopic PC-3 tumors . M-LYVE-1-positive staining was observed primarily in the tumor periphery and in the peritumoral area (A-B). No differences were detected in the density of lymphatic vessels Bar 500 μm.

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Staining

    Metastasis of PC-3/VEGF-C tumors to prostate-draining lymph nodes and lungs . The prostate draining lymph nodes and the lungs were cut through to detect metastasis. Altogether 8-10 lymph nodes and six lung sections/mouse were studied and number of metastases was counted. The relative metastatic area of lymph nodes was determined by histomorphometry but there were no statistically significant differences (data not shown). The occurrence of metastasis in lymph nodes was 21% ( n = 6 mice out of 29 tumor-bearing mice) in the PC-3/VEGF-C group and 58% ( n = 14 mice out of 24 tumor-bearing mice) in the PC-3/mock group and in lungs was 48% ( n = 14 out of 29 tumor bearing mice) in the PC-3/VEGF-C group and 8% ( n = 2 out of 24 tumor-bearing mice) in the PC-3/mock group.

    Journal: BMC Cancer

    Article Title: Overexpression of vascular endothelial growth factor C increases growth and alters the metastatic pattern of orthotopic PC-3 prostate tumors

    doi: 10.1186/1471-2407-9-362

    Figure Lengend Snippet: Metastasis of PC-3/VEGF-C tumors to prostate-draining lymph nodes and lungs . The prostate draining lymph nodes and the lungs were cut through to detect metastasis. Altogether 8-10 lymph nodes and six lung sections/mouse were studied and number of metastases was counted. The relative metastatic area of lymph nodes was determined by histomorphometry but there were no statistically significant differences (data not shown). The occurrence of metastasis in lymph nodes was 21% ( n = 6 mice out of 29 tumor-bearing mice) in the PC-3/VEGF-C group and 58% ( n = 14 mice out of 24 tumor-bearing mice) in the PC-3/mock group and in lungs was 48% ( n = 14 out of 29 tumor bearing mice) in the PC-3/VEGF-C group and 8% ( n = 2 out of 24 tumor-bearing mice) in the PC-3/mock group.

    Article Snippet: VEGF-C protein concentrations from cell lysates and 24 h conditioned media of cell clones were further quantified by ELISA (Bender MedSystems, Vienna, Austria) according to the manufacturer's instructions.

    Techniques: Mouse Assay