anti human cd31 antibody  (Thermo Fisher)


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    Structured Review

    Thermo Fisher anti human cd31 antibody
    FISH analysis in human RCC and normal renal tissue sections. A: CA IX immunostaining in RCC tissue and normal kidney tissue. Upper panels show <t>CD31</t> staining in vascular ECs. Lower panels show that CA IX was expressed in tumor cells in RCC tissue but not
    Anti Human Cd31 Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 2 article reviews
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    anti human cd31 antibody - by Bioz Stars, 2022-09
    99/100 stars

    Images

    1) Product Images from "Cytogenetic Abnormalities of Tumor-Associated Endothelial Cells in Human Malignant Tumors"

    Article Title: Cytogenetic Abnormalities of Tumor-Associated Endothelial Cells in Human Malignant Tumors

    Journal: The American Journal of Pathology

    doi: 10.2353/ajpath.2009.090202

    FISH analysis in human RCC and normal renal tissue sections. A: CA IX immunostaining in RCC tissue and normal kidney tissue. Upper panels show CD31 staining in vascular ECs. Lower panels show that CA IX was expressed in tumor cells in RCC tissue but not
    Figure Legend Snippet: FISH analysis in human RCC and normal renal tissue sections. A: CA IX immunostaining in RCC tissue and normal kidney tissue. Upper panels show CD31 staining in vascular ECs. Lower panels show that CA IX was expressed in tumor cells in RCC tissue but not

    Techniques Used: Fluorescence In Situ Hybridization, Immunostaining, Staining

    FISH analysis in freshly isolated and cytospun hTECs and hNECs. A and B: FISH analysis of freshly isolated and cytospun hTECs and hNECs. hTECs ( A ) and hNECs ( B ) were stained for CD31, VE-cadherin, or the RCC marker CA IX. FISH was performed using chromosome
    Figure Legend Snippet: FISH analysis in freshly isolated and cytospun hTECs and hNECs. A and B: FISH analysis of freshly isolated and cytospun hTECs and hNECs. hTECs ( A ) and hNECs ( B ) were stained for CD31, VE-cadherin, or the RCC marker CA IX. FISH was performed using chromosome

    Techniques Used: Fluorescence In Situ Hybridization, Isolation, Staining, Marker

    FISH analysis in uncultured and cultured mTECs and mNECs. mTECs isolated from xenografts of human epithelial tumors were aneuploid. Cultured and uncultured mTECs were positive for CD31 (green). Nuclei were counterstained with DAPI (blue). Three or more
    Figure Legend Snippet: FISH analysis in uncultured and cultured mTECs and mNECs. mTECs isolated from xenografts of human epithelial tumors were aneuploid. Cultured and uncultured mTECs were positive for CD31 (green). Nuclei were counterstained with DAPI (blue). Three or more

    Techniques Used: Fluorescence In Situ Hybridization, Cell Culture, Isolation

    2) Product Images from "Hypoxia-induced factor-1 alpha upregulates vascular endothelial growth factor C to promote lymphangiogenesis and angiogenesis in breast cancer patients"

    Article Title: Hypoxia-induced factor-1 alpha upregulates vascular endothelial growth factor C to promote lymphangiogenesis and angiogenesis in breast cancer patients

    Journal: Journal of Biomedical Research

    doi: 10.7555/JBR.27.20130021

    Immunohistochemical staining of D2-40 and CD31. A: Immunoreactivity of D2-40 proteins was observed in the cytoplasm and cellular membrane of lymphatic endothelial cells (magnification×200). D2-40 expression was restricted to thin-walled lymphatic vessels containing no red blood cells (arrows). D2-40-positive cells were largely distributed in peritumoral tissue (hot spot). B: Representative sections showing CD31+ staining in blood microvessels/endothelial cells (magnification×400).
    Figure Legend Snippet: Immunohistochemical staining of D2-40 and CD31. A: Immunoreactivity of D2-40 proteins was observed in the cytoplasm and cellular membrane of lymphatic endothelial cells (magnification×200). D2-40 expression was restricted to thin-walled lymphatic vessels containing no red blood cells (arrows). D2-40-positive cells were largely distributed in peritumoral tissue (hot spot). B: Representative sections showing CD31+ staining in blood microvessels/endothelial cells (magnification×400).

    Techniques Used: Immunohistochemistry, Staining, Expressing

    3) Product Images from "In Vivo Evaluation of Gamma-Irradiated and Heparin-Immobilized Small-Diameter Polycaprolactone Vascular Grafts with VEGF in Aged Rats"

    Article Title: In Vivo Evaluation of Gamma-Irradiated and Heparin-Immobilized Small-Diameter Polycaprolactone Vascular Grafts with VEGF in Aged Rats

    Journal: Polymers

    doi: 10.3390/polym14061265

    Representative immunohistochemistry images of a normal rat (( A , E ) n = 3), PCL (( B , F ) n = 4), H-PCL (( C , G ) n = 4), and VH-PCL groups (( D , H ) n = 4) at 12 weeks post-implantation in aged rats: ( A – D ) Green = CD31; blue = DAPI; ( E – H ) Green = α-SMA; blue = DAPI. L, lumen; PCL, poly(ε-caprolactone); H-PCL, heparin-AEMA-PCL; AEMA, 2-aminoethyl methacrylate; VH-PCL, vascular endothelial growth factor (VEGF)-loaded heparin-AEMA-PCL; DAPI, 4′,6-diamidino-2-phenylindole; α-SMA, alpha–smooth muscle actin.
    Figure Legend Snippet: Representative immunohistochemistry images of a normal rat (( A , E ) n = 3), PCL (( B , F ) n = 4), H-PCL (( C , G ) n = 4), and VH-PCL groups (( D , H ) n = 4) at 12 weeks post-implantation in aged rats: ( A – D ) Green = CD31; blue = DAPI; ( E – H ) Green = α-SMA; blue = DAPI. L, lumen; PCL, poly(ε-caprolactone); H-PCL, heparin-AEMA-PCL; AEMA, 2-aminoethyl methacrylate; VH-PCL, vascular endothelial growth factor (VEGF)-loaded heparin-AEMA-PCL; DAPI, 4′,6-diamidino-2-phenylindole; α-SMA, alpha–smooth muscle actin.

    Techniques Used: Immunohistochemistry

    4) Product Images from "Non–beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma"

    Article Title: Non–beta blocker enantiomers of propranolol and atenolol inhibit vasculogenesis in infantile hemangioma

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI151109

    R(+) propranolol does not affect HemSC to HemPericyte differentiation. ( A ) HemSCs and HemECs (1:1) were suspended in Matrigel and injected into nude mice, with 2 implants/mouse ( n = 8 mice). The mice were treated with 5 mg/kg R(+) propranolol or an equivalent volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panel of the images. Scale bars: 10 mm. H E staining showed similar vessel density in the implants of R(+) propranolol–treated mice compared with vessel density in the implants of control mice (middle panels). Scale bars: 100 μm. Anti–human CD31 staining (red) confirmed the similar number of blood vessels in R(+) propranolol–treated mice and control mice (bottom panels). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. P values were calculated using a 2-tailed, unpaired Student’s t test. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per group. ( B ) Implant sections stained with UEA I (green) and anti-αSMA (red) showed similar pericyte coverage per vessel area in mice treated with PBS ( n = 7 mice) or R(+) propranolol ( n = 6 mice). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. P values were calculated by 2-tailed, unpaired Student’s t test. Only implants showing vessel formation were used for further analysis [ n = 7 PBS implants; n = 6 R(+) propranolol implants]. Graphs show quantification of vessels/mm 2 in the H E-stained sections (top), human CD31 + vessels/mm 2 (middle), and pericytes/vessel area (bottom). ( C ) qPCR showed that treatment with propranolol or its R(+) enantiomers (10 μM) did not affect the expression of pericyte markers (calponin, PDGFRβ, and αSMA) in HemSCs cocultured with HemECs. Coculturing was conducted for 5 days: CD31 + cells were removed by magnetic beads before RNA extraction of the CD31 – cells as shown in the schematic. DAPT (10 μM) served as a positive control. Data from 3 independent experiments were plotted. Statistical significance was determined by 1-way ANOVA with Dunnett’s multiple-comparison test. P values can be found in Supplemental Figure 2C . Data in all graphs show the mean ± SD.
    Figure Legend Snippet: R(+) propranolol does not affect HemSC to HemPericyte differentiation. ( A ) HemSCs and HemECs (1:1) were suspended in Matrigel and injected into nude mice, with 2 implants/mouse ( n = 8 mice). The mice were treated with 5 mg/kg R(+) propranolol or an equivalent volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panel of the images. Scale bars: 10 mm. H E staining showed similar vessel density in the implants of R(+) propranolol–treated mice compared with vessel density in the implants of control mice (middle panels). Scale bars: 100 μm. Anti–human CD31 staining (red) confirmed the similar number of blood vessels in R(+) propranolol–treated mice and control mice (bottom panels). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. P values were calculated using a 2-tailed, unpaired Student’s t test. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per group. ( B ) Implant sections stained with UEA I (green) and anti-αSMA (red) showed similar pericyte coverage per vessel area in mice treated with PBS ( n = 7 mice) or R(+) propranolol ( n = 6 mice). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. P values were calculated by 2-tailed, unpaired Student’s t test. Only implants showing vessel formation were used for further analysis [ n = 7 PBS implants; n = 6 R(+) propranolol implants]. Graphs show quantification of vessels/mm 2 in the H E-stained sections (top), human CD31 + vessels/mm 2 (middle), and pericytes/vessel area (bottom). ( C ) qPCR showed that treatment with propranolol or its R(+) enantiomers (10 μM) did not affect the expression of pericyte markers (calponin, PDGFRβ, and αSMA) in HemSCs cocultured with HemECs. Coculturing was conducted for 5 days: CD31 + cells were removed by magnetic beads before RNA extraction of the CD31 – cells as shown in the schematic. DAPT (10 μM) served as a positive control. Data from 3 independent experiments were plotted. Statistical significance was determined by 1-way ANOVA with Dunnett’s multiple-comparison test. P values can be found in Supplemental Figure 2C . Data in all graphs show the mean ± SD.

    Techniques Used: Injection, Mouse Assay, Staining, Real-time Polymerase Chain Reaction, Expressing, Magnetic Beads, RNA Extraction, Positive Control

    R(+) atenolol inhibits hemangioma endothelial differentiation in vitro and vessel formation in vivo. ( A ) Atenolol and its purified R(+) enantiomer, both tested at 5 μM, inhibited endothelial differentiation of HemSCs isolated from 2 IH tumor specimens as effectively as did R(+) propranolol. R(+) propranolol served as a positive control for inhibition. The endothelial differentiation markers CD31 and VE-cadherin and the hemangioma endothelial markers NOTCH1, PlexinD1, and VEGFR1 under each treatment condition in 3 biological replicates, determined by qPCR, were standardized as previously described (76 ). The HemSC-to-endothelial differentiation assay was conducted 2 separate times with HemSC 167 and once with HemSC 165, providing 3 data points. Statistical significance was determined by 1-way ANOVA with Bonferroni’s post hoc test. P values are listed in Supplemental Figure 3 . ( B ) HemSCs were pretreated with PBS, 10 μM atenolol, or 10 μM R(+) atenolol 24 hours before the experiment and were then suspended in Matrigel with PBS, 5 μM atenolol, or 5 μM R(+) atenolol and injected into nude mice, with 2 implants per mouse (see schematic in Figure 1A ; n = 16 PBS-treated HemSCs, n = 8 atenolol-treated HemSCs, n = 8 R(+) atenolol–treated HemSCs). The mice were treated with 5 mg/kg atenolol, 5 mg/kg R(+) atenolol, or an equal volume of PBS twice a day. Matrigel implants harvested after 7 days are shown in the top panels of the images. Scale bars: 10 mm. Images also show H E staining (middle panels) and anti–human CD31 staining (red, bottom panels), with nuclei counterstained with DAPI (blue). Scale bars: 100 μm. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per treatment group and 16 in the control group. ( C ) Quantification of vessel density based on H E staining (middle panels) and anti–human CD31 staining (bottom panels) showed a significant reduction in vessel density in the implants of atenolol- and R(+) atenolol–treated mice versus implants of control mice. Statistical analysis was performed using 1-way ANOVA with Dunnett’s multiple-comparison test.
    Figure Legend Snippet: R(+) atenolol inhibits hemangioma endothelial differentiation in vitro and vessel formation in vivo. ( A ) Atenolol and its purified R(+) enantiomer, both tested at 5 μM, inhibited endothelial differentiation of HemSCs isolated from 2 IH tumor specimens as effectively as did R(+) propranolol. R(+) propranolol served as a positive control for inhibition. The endothelial differentiation markers CD31 and VE-cadherin and the hemangioma endothelial markers NOTCH1, PlexinD1, and VEGFR1 under each treatment condition in 3 biological replicates, determined by qPCR, were standardized as previously described (76 ). The HemSC-to-endothelial differentiation assay was conducted 2 separate times with HemSC 167 and once with HemSC 165, providing 3 data points. Statistical significance was determined by 1-way ANOVA with Bonferroni’s post hoc test. P values are listed in Supplemental Figure 3 . ( B ) HemSCs were pretreated with PBS, 10 μM atenolol, or 10 μM R(+) atenolol 24 hours before the experiment and were then suspended in Matrigel with PBS, 5 μM atenolol, or 5 μM R(+) atenolol and injected into nude mice, with 2 implants per mouse (see schematic in Figure 1A ; n = 16 PBS-treated HemSCs, n = 8 atenolol-treated HemSCs, n = 8 R(+) atenolol–treated HemSCs). The mice were treated with 5 mg/kg atenolol, 5 mg/kg R(+) atenolol, or an equal volume of PBS twice a day. Matrigel implants harvested after 7 days are shown in the top panels of the images. Scale bars: 10 mm. Images also show H E staining (middle panels) and anti–human CD31 staining (red, bottom panels), with nuclei counterstained with DAPI (blue). Scale bars: 100 μm. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per treatment group and 16 in the control group. ( C ) Quantification of vessel density based on H E staining (middle panels) and anti–human CD31 staining (bottom panels) showed a significant reduction in vessel density in the implants of atenolol- and R(+) atenolol–treated mice versus implants of control mice. Statistical analysis was performed using 1-way ANOVA with Dunnett’s multiple-comparison test.

    Techniques Used: In Vitro, In Vivo, Purification, Isolation, Positive Control, Inhibition, Real-time Polymerase Chain Reaction, Differentiation Assay, Injection, Mouse Assay, Staining

    The orally active SOX18 inhibitor Sm4 suppresses vessel formation in a murine model for IH. HemSCs were pretreated with 10% DMSO in PBS or 10 μM Sm4 for 24 hours, suspended in Matrigel with 10% DMSO in PBS or 5 μM Sm4 and injected into nude mice, with 2 implants per mouse ( n = 12). The mice were treated with 25 mg/kg Sm4 or an equivalent volume of 10% DMSO in PBS once a day by oral gavage. Matrigel implants harvested after 7 days are shown in the top panels. Scale bars: 10 mm. H E staining (middle panels) and anti–human CD31 staining (red; lower panels) showed a significant reduction in vessel density in the implants from Sm4-treated mice compared with those from cont rol mice. Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. Graphs show quantification of vessels/mm 2 in the H E-stained sections (top) and human CD31 + vessels/mm 2 (bottom). P values were calculated by 2-tailed, unpaired Students’ t test. Data show the mean ± SD. Data were collected for 2 implants in each of 6 mice, leading to an observation sample size of 12 per group.
    Figure Legend Snippet: The orally active SOX18 inhibitor Sm4 suppresses vessel formation in a murine model for IH. HemSCs were pretreated with 10% DMSO in PBS or 10 μM Sm4 for 24 hours, suspended in Matrigel with 10% DMSO in PBS or 5 μM Sm4 and injected into nude mice, with 2 implants per mouse ( n = 12). The mice were treated with 25 mg/kg Sm4 or an equivalent volume of 10% DMSO in PBS once a day by oral gavage. Matrigel implants harvested after 7 days are shown in the top panels. Scale bars: 10 mm. H E staining (middle panels) and anti–human CD31 staining (red; lower panels) showed a significant reduction in vessel density in the implants from Sm4-treated mice compared with those from cont rol mice. Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. Graphs show quantification of vessels/mm 2 in the H E-stained sections (top) and human CD31 + vessels/mm 2 (bottom). P values were calculated by 2-tailed, unpaired Students’ t test. Data show the mean ± SD. Data were collected for 2 implants in each of 6 mice, leading to an observation sample size of 12 per group.

    Techniques Used: Injection, Mouse Assay, Staining

    R(+) propranolol and R(+) atenolol inhibit IH vasculogenesis but not body weight or glucose levels. ( A ) HemSCs were pretreated with PBS or 10 μM treatment drug 24 hours before the experiment, suspended in Matrigel with PBS or 5 μM treatment drug, and injected into nude mice, with 2 implants/mouse [ n = 10 PBS-treated mice, n = 8 propranolol-treated mice, n = 8 R(+) propranolol–treated mice, n = 10 R(+) atenolol–treated mice]. The mice were treated with 12.5 mg/kg propranolol, 12.5 mg/kg R(+) propranolol, 12.5 mg/kg R(+) atenolol, or an equal volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panels of th images. The PBS control implants in A are also shown in Figure 3A , because the 5 mg/kg atenolol group shown in Figure 3B was run at the same time as the groups in A . Scale bars: 10 mm. Images show H E staining (middle panels) and anti–human CD31 staining (red; bottom panels), with nuclei counterstained with DAPI (blue). Scale bars: 100 μm. ( B ) Quantification of vessel density based on H E staining ( A , middle panels) and anti–human CD31 staining ( A , bottom panels) showed that R(+) atenolol was as effective as R(+) propranolol and propranolol in inhibiting vessel formation. Statistical significance was determined by 1-way ANOVA with Dunnett’s multiple-comparison test. P values are listed in the table in Supplemental Figure 5E . ( C ) Body weight and glucose levels were measured daily. Neither propranolol, R(+) propranolol, or R(+) atenolol affected body weight or glucose levels of nude mice. Data show the mean ± SD in all graphs. Data were collected for 2 implants in each mouse, leading to an observation sample size of 8 in the propranolol and R(+) propranolol treatment groups and 10 in the atenolol and PBS control groups.
    Figure Legend Snippet: R(+) propranolol and R(+) atenolol inhibit IH vasculogenesis but not body weight or glucose levels. ( A ) HemSCs were pretreated with PBS or 10 μM treatment drug 24 hours before the experiment, suspended in Matrigel with PBS or 5 μM treatment drug, and injected into nude mice, with 2 implants/mouse [ n = 10 PBS-treated mice, n = 8 propranolol-treated mice, n = 8 R(+) propranolol–treated mice, n = 10 R(+) atenolol–treated mice]. The mice were treated with 12.5 mg/kg propranolol, 12.5 mg/kg R(+) propranolol, 12.5 mg/kg R(+) atenolol, or an equal volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panels of th images. The PBS control implants in A are also shown in Figure 3A , because the 5 mg/kg atenolol group shown in Figure 3B was run at the same time as the groups in A . Scale bars: 10 mm. Images show H E staining (middle panels) and anti–human CD31 staining (red; bottom panels), with nuclei counterstained with DAPI (blue). Scale bars: 100 μm. ( B ) Quantification of vessel density based on H E staining ( A , middle panels) and anti–human CD31 staining ( A , bottom panels) showed that R(+) atenolol was as effective as R(+) propranolol and propranolol in inhibiting vessel formation. Statistical significance was determined by 1-way ANOVA with Dunnett’s multiple-comparison test. P values are listed in the table in Supplemental Figure 5E . ( C ) Body weight and glucose levels were measured daily. Neither propranolol, R(+) propranolol, or R(+) atenolol affected body weight or glucose levels of nude mice. Data show the mean ± SD in all graphs. Data were collected for 2 implants in each mouse, leading to an observation sample size of 8 in the propranolol and R(+) propranolol treatment groups and 10 in the atenolol and PBS control groups.

    Techniques Used: Injection, Mouse Assay, Staining

    R(+) propranolol inhibits vessel formation in a murine model for IH. ( A ) HemSCs were pretreated with PBS or 10 μM R(+) propranolol for 24 hours, suspended in Matrigel with PBS or 5 μM R(+) propranolol, and then injected into nude mice, with 2 implants/mouse ( n = 8 mice). The mice were treated with 5 mg/kg R(+) propranolol or an equivalent volume of PBS twice a day as depicted in the schematic. Matrigel implants harvested after 7 days are shown in the top panel of the images. Scale bars: 10 mm. H E staining indicated fewer blood vessels in the implants of R(+) propranolol–treated mice compared with implants in the control mice (middle panels). Scale bars: 100 μm. Anti–human CD31 staining (red) confirmed the reduced vessel density in R(+) propranolol–treated mice compared with vessel density in control mice (bottom panels). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. Graphs show quantification of vessels/mm 2 in the H E-stained sections (left) and human CD31 + vessels/mm 2 (right). ( B ) HemSCs were treated as described in A . Mice were treated with 12.5 mg/kg R(+) propranolol or the equivalent volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panel of the images, with 2 implants/mouse ( n = 8 mice). Scale bars: 10 mm. H E staining (middle panels) and anti–human CD31 staining (red; bottom panels) showed a significant reduction in vessel density in the implants of R(+) propranolol–treated mice compared with control mice. Scale bars: 100 μm. P values were calculated using a 2-tailed, unpaired Student’s t test. Data show the mean ± SD. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per group.
    Figure Legend Snippet: R(+) propranolol inhibits vessel formation in a murine model for IH. ( A ) HemSCs were pretreated with PBS or 10 μM R(+) propranolol for 24 hours, suspended in Matrigel with PBS or 5 μM R(+) propranolol, and then injected into nude mice, with 2 implants/mouse ( n = 8 mice). The mice were treated with 5 mg/kg R(+) propranolol or an equivalent volume of PBS twice a day as depicted in the schematic. Matrigel implants harvested after 7 days are shown in the top panel of the images. Scale bars: 10 mm. H E staining indicated fewer blood vessels in the implants of R(+) propranolol–treated mice compared with implants in the control mice (middle panels). Scale bars: 100 μm. Anti–human CD31 staining (red) confirmed the reduced vessel density in R(+) propranolol–treated mice compared with vessel density in control mice (bottom panels). Nuclei were counterstained with DAPI (blue). Scale bars: 100 μm. Graphs show quantification of vessels/mm 2 in the H E-stained sections (left) and human CD31 + vessels/mm 2 (right). ( B ) HemSCs were treated as described in A . Mice were treated with 12.5 mg/kg R(+) propranolol or the equivalent volume of PBS twice a day. Matrigel implants harvested after 7 days are displayed in the top panel of the images, with 2 implants/mouse ( n = 8 mice). Scale bars: 10 mm. H E staining (middle panels) and anti–human CD31 staining (red; bottom panels) showed a significant reduction in vessel density in the implants of R(+) propranolol–treated mice compared with control mice. Scale bars: 100 μm. P values were calculated using a 2-tailed, unpaired Student’s t test. Data show the mean ± SD. Data were collected for 2 implants in each of 4 mice, leading to an observation sample size of 8 per group.

    Techniques Used: Injection, Mouse Assay, Staining

    5) Product Images from "Suppression of tumor angiogenesis by metformin treatment via a mechanism linked to targeting of HER2/HIF-1α/VEGF secretion axis"

    Article Title: Suppression of tumor angiogenesis by metformin treatment via a mechanism linked to targeting of HER2/HIF-1α/VEGF secretion axis

    Journal: Oncotarget

    doi:

    Inhibition of VEGFA signaling was involved in the mechanism of metformin-induced anti-angiogenesis and reduction of vessel leakage A, B. Immunoblotting for protein expression of VEGF 165 in MCF-7, MDA-MB-231 and MDA-MB-453 cells untreated or treated with metformin, HRG-β1 or the combined treatment for 24 h. 50 μg protein per lane. C. Thirty minutes before mice were sacrificed, 100 mg/kg Fitc-conjugated Dextran (70 kD) in 100 μl was intravenously injected. CD31. Fitc signaling (Green) outside the boundary of TRITC signaling (Red) was considered as the dextran leaking outside the tumor vessel. D. The tumor cell-conditioned medium (TCM) of MDA-MB-453 cells with or without HRG-β1 pretreatment was pre-incubated with bevacizumab (250 μg/ml) for 1 h. Human umbilical endothelial cells (HUVECs) were then cultured with the mixture of TCM and BEV and finally the cellular viability was determined ( n = 6). E. Human recombinant VEGFA (10 ng/ml) was first added to the TCM of MDA-MB-453 cells without or with metformin pretreatment. After that, HUVECs were cultured with MDA-MB-453 TCM or the mixture of TCM and supplemented VEGFA ( n = 6). All data is presented as mean ± S.E.M. * p
    Figure Legend Snippet: Inhibition of VEGFA signaling was involved in the mechanism of metformin-induced anti-angiogenesis and reduction of vessel leakage A, B. Immunoblotting for protein expression of VEGF 165 in MCF-7, MDA-MB-231 and MDA-MB-453 cells untreated or treated with metformin, HRG-β1 or the combined treatment for 24 h. 50 μg protein per lane. C. Thirty minutes before mice were sacrificed, 100 mg/kg Fitc-conjugated Dextran (70 kD) in 100 μl was intravenously injected. CD31. Fitc signaling (Green) outside the boundary of TRITC signaling (Red) was considered as the dextran leaking outside the tumor vessel. D. The tumor cell-conditioned medium (TCM) of MDA-MB-453 cells with or without HRG-β1 pretreatment was pre-incubated with bevacizumab (250 μg/ml) for 1 h. Human umbilical endothelial cells (HUVECs) were then cultured with the mixture of TCM and BEV and finally the cellular viability was determined ( n = 6). E. Human recombinant VEGFA (10 ng/ml) was first added to the TCM of MDA-MB-453 cells without or with metformin pretreatment. After that, HUVECs were cultured with MDA-MB-453 TCM or the mixture of TCM and supplemented VEGFA ( n = 6). All data is presented as mean ± S.E.M. * p

    Techniques Used: Inhibition, Expressing, Multiple Displacement Amplification, Mouse Assay, Injection, Incubation, Cell Culture, Recombinant

    Inhibition of HIF-1α greatly contributed to metformin-induced VEGF down-regulation in the presence of HER2 signaling MDA-MB-453 cells were cultured with metformin (10 mM), AG825 (10 μM), YC-1 (10 μM) or HRG-β1 (50 ng/ml) for 24 h, then the intracellular proteins, mRNA, and tumor cell-conditioned medium (TCM) were extracted. A. YC-1 almost completely inhibited HIF-1α expression of MDA-MB-453 cells even in the presence of HRG-β1 treatment. Representative image showing mRNA levels of B. HIF-1α and C. VEGFA in MDA-MB-453 cells ( n = 5 for both). D. HUVECs were cultured with serum-free medium (SFM) or TCM from MDA-MB-453 cells treated with YC-1 (10 μM), HRG-β1 (50 ng/ml) or both ( n = 6). E. Immunoblotting for protein expression of HIF-1α in MDA-MB-453 cells in both the presence and absence of MG132 (20 μM). F. Immunohistochemical staining for HIF-1α in 4T1 tumors from control mice or those treated with metformin (200 mg/kg • day), YC-1 (10 mg/kg. day), or AG825 (10 mg/kg. day). Red arrows indicate the cells with nuclei positive for HIF-1α. Scale bar: 100 μm. G. Immunofluorescent double staining for CD31 and HIF-1α in 4T1 tumors. Scale bar: 100 μm. All data is presented as mean ± S.E.M. * p
    Figure Legend Snippet: Inhibition of HIF-1α greatly contributed to metformin-induced VEGF down-regulation in the presence of HER2 signaling MDA-MB-453 cells were cultured with metformin (10 mM), AG825 (10 μM), YC-1 (10 μM) or HRG-β1 (50 ng/ml) for 24 h, then the intracellular proteins, mRNA, and tumor cell-conditioned medium (TCM) were extracted. A. YC-1 almost completely inhibited HIF-1α expression of MDA-MB-453 cells even in the presence of HRG-β1 treatment. Representative image showing mRNA levels of B. HIF-1α and C. VEGFA in MDA-MB-453 cells ( n = 5 for both). D. HUVECs were cultured with serum-free medium (SFM) or TCM from MDA-MB-453 cells treated with YC-1 (10 μM), HRG-β1 (50 ng/ml) or both ( n = 6). E. Immunoblotting for protein expression of HIF-1α in MDA-MB-453 cells in both the presence and absence of MG132 (20 μM). F. Immunohistochemical staining for HIF-1α in 4T1 tumors from control mice or those treated with metformin (200 mg/kg • day), YC-1 (10 mg/kg. day), or AG825 (10 mg/kg. day). Red arrows indicate the cells with nuclei positive for HIF-1α. Scale bar: 100 μm. G. Immunofluorescent double staining for CD31 and HIF-1α in 4T1 tumors. Scale bar: 100 μm. All data is presented as mean ± S.E.M. * p

    Techniques Used: Inhibition, Multiple Displacement Amplification, Cell Culture, Expressing, Immunohistochemistry, Staining, Mouse Assay, Double Staining

    Inhibitory effects of metformin on tumor angiogenesis and HER2 activity In the 4T1 breast carcinoma model, the BALB/C mice were orally administrated with metformin (200 mg/kg • day) or drinking water (control) for 14 days after the average tumor volume reached 100 mm 3 . A. Representative 3D-reconstruction image for detecting CD31 + vessels in 4T1 tumors. White stars and arrows indicate the dilated vessels and vascular sprouts, respectively. Scale, 50 μm. B. Quantification of microvessel density in 4T1 tumor sections ( n = 8). C. Representative image showing the frequency distribution of vessel diameter in 4T1 tumors ( n = 8). D. Immunohistochemical staining for protein expression of phospho-HER2 (Tyr 1221/1222) in 4T1 tumors. Scale, 50 μm. E. Immunoblotting for both total and phosphorylated levels of HER2 protein in 4T1 and MDA-MB-453 cell cells untreated or treated with 10 mM metformin. 80 μg protein per lane. Quantification of the final weight F. and growth curve G. of 4T1 tumors from mice untreated or treated with metformin (200 mg/kg • day). All data is presented as mean ± S.E.M. * p
    Figure Legend Snippet: Inhibitory effects of metformin on tumor angiogenesis and HER2 activity In the 4T1 breast carcinoma model, the BALB/C mice were orally administrated with metformin (200 mg/kg • day) or drinking water (control) for 14 days after the average tumor volume reached 100 mm 3 . A. Representative 3D-reconstruction image for detecting CD31 + vessels in 4T1 tumors. White stars and arrows indicate the dilated vessels and vascular sprouts, respectively. Scale, 50 μm. B. Quantification of microvessel density in 4T1 tumor sections ( n = 8). C. Representative image showing the frequency distribution of vessel diameter in 4T1 tumors ( n = 8). D. Immunohistochemical staining for protein expression of phospho-HER2 (Tyr 1221/1222) in 4T1 tumors. Scale, 50 μm. E. Immunoblotting for both total and phosphorylated levels of HER2 protein in 4T1 and MDA-MB-453 cell cells untreated or treated with 10 mM metformin. 80 μg protein per lane. Quantification of the final weight F. and growth curve G. of 4T1 tumors from mice untreated or treated with metformin (200 mg/kg • day). All data is presented as mean ± S.E.M. * p

    Techniques Used: Activity Assay, Mouse Assay, Immunohistochemistry, Staining, Expressing, Multiple Displacement Amplification

    AG825 decreased HER2 signaling-induced VEGF expression and suppressed tumor angiogenesis MDA-MB-453 or 4T1 cells were cultured with metformin (10 mM), AG825 (10 μM) or HRG-β1 (50 ng/ml) in DMEM containing 10% FBS for 24 h, then the intracellular proteins, mRNA and TCM were extracted. A. Immunoblotting for the total and phosphorylated levels (Tyr 1221/1222) of HER2 and VEGFA proteins in MDA-MB-453 cells. B. Representative images showing the mRNA and secretion levels of VEGF of MDA-MB-453 cells ( n = 5 for both). C. Representative image showing the growth curve of 4T1 tumors from control mice and those treated with metformin (200 mg/kg • day), or AG825 (10 mg/kg. day) ( n = 6 − 8). D. Immunohistochemical staining for VEGFA in 4T1 tumors; scale, 200 μm. E. Immunohistochemical staining for CD31 + vessels and quantitative measurement of microvessel density in 4T1 tumors ( n = 6 − 8). Scale bar, 75 μm. All data is presented as mean ± S.E.M. * p
    Figure Legend Snippet: AG825 decreased HER2 signaling-induced VEGF expression and suppressed tumor angiogenesis MDA-MB-453 or 4T1 cells were cultured with metformin (10 mM), AG825 (10 μM) or HRG-β1 (50 ng/ml) in DMEM containing 10% FBS for 24 h, then the intracellular proteins, mRNA and TCM were extracted. A. Immunoblotting for the total and phosphorylated levels (Tyr 1221/1222) of HER2 and VEGFA proteins in MDA-MB-453 cells. B. Representative images showing the mRNA and secretion levels of VEGF of MDA-MB-453 cells ( n = 5 for both). C. Representative image showing the growth curve of 4T1 tumors from control mice and those treated with metformin (200 mg/kg • day), or AG825 (10 mg/kg. day) ( n = 6 − 8). D. Immunohistochemical staining for VEGFA in 4T1 tumors; scale, 200 μm. E. Immunohistochemical staining for CD31 + vessels and quantitative measurement of microvessel density in 4T1 tumors ( n = 6 − 8). Scale bar, 75 μm. All data is presented as mean ± S.E.M. * p

    Techniques Used: Expressing, Multiple Displacement Amplification, Cell Culture, Mouse Assay, Immunohistochemistry, Staining

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    Thermo Fisher cd31
    Comparison of kappa values among pathologists for lymphovascular invasion (LVI) detection in colorectal cancers. While the average of LVI detection rate for each pathologist was 43% with hematoxylin and eosin (H E) only, 10% with <t>CD31,</t> 29% with D2-40, and 16% with ERG, the consensus reached 80% of LVI detection after a joint discussion about ERG patterns with LVI. a Interpreted by ERG
    Cd31, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    99
    Thermo Fisher anti pecam 1 mab conjugated
    Chemoattractants stimulate release of TNF from neutrophils in vitro and in vivo. Mixed mouse blood leukocytes were treated with PBS (control) or stimulated with LTB 4 (10 or 30 min). Supernatants were assayed for soluble TNF by ELISA and cells were permeabilized and immunostained for analysis of intracellular TNF by flow cytometry and confocal microscopy. (A) Representative flow cytometry histograms from 4 independent experiments showing the binding of anti-TNF mAb (black lines) or control IgG (filled). (B) Quantification of intracellular TNF by flow cytometry (expressed as RFI; n = 6 blood samples for PBS and 30 min LTB 4 , n = 5 for 10 min LTB 4 ) from 4 independent experiments. (C) Quantification of released TNF ( n = 4) from 4 independent experiments. ND, not detected. (D) Representative confocal images of neutrophils from two independent experiments show cells treated with PBS or LTB 4 (10 and 30 min) and stained for the neutrophil marker MRP-14 (green) or TNF (red). Bar, 5 µm. (E) Representative 3D-reconstructed images of LTB 4 -stimulated cremasteric postcapillary venule (luminal side) showing GFP-neutrophils and <t>PECAM-1–labeled</t> ECs (red). The top panel shows neutrophils at different steps of the transmigration response, i.e., luminal crawling, preTEM phase (6 min before breaching ECs), TEM phase, and abluminal crawling. The associated TNF detected on the leukocyte surface for each step (intensity rainbow color code from blue [low intensity] to red [high intensity]) is shown in the bottom panels with and without the associated neutrophil. Bar, 5 µm. (F) Mean fluorescent intensity of signals on neutrophils was quantified in mice injected with anti-TNF or control mAbs ( n = 4 mice/group) from 4 independent experiments. A total of ∼40 neutrophils were tracked and analyzed for each group. All data are means ± SEM. Statistical differences from PBS (B and C), signals from luminal crawling cells (F), or other comparisons (indicated by lines) are shown by asterisks. *, P
    Anti Pecam 1 Mab Conjugated, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Comparison of kappa values among pathologists for lymphovascular invasion (LVI) detection in colorectal cancers. While the average of LVI detection rate for each pathologist was 43% with hematoxylin and eosin (H E) only, 10% with CD31, 29% with D2-40, and 16% with ERG, the consensus reached 80% of LVI detection after a joint discussion about ERG patterns with LVI. a Interpreted by ERG

    Journal: Korean Journal of Pathology

    Article Title: ERG Immunohistochemistry as an Endothelial Marker for Assessing Lymphovascular Invasion

    doi: 10.4132/KoreanJPathol.2013.47.4.355

    Figure Lengend Snippet: Comparison of kappa values among pathologists for lymphovascular invasion (LVI) detection in colorectal cancers. While the average of LVI detection rate for each pathologist was 43% with hematoxylin and eosin (H E) only, 10% with CD31, 29% with D2-40, and 16% with ERG, the consensus reached 80% of LVI detection after a joint discussion about ERG patterns with LVI. a Interpreted by ERG

    Article Snippet: Primary antibodies were CD31 (1:25, Thermo Fisher Scientific Inc., Kalamazoo, MI, USA), D2-40 (predilution, Dako, Glostrup, Denmark), and ERG (predilution, Biocare Medical, Concord, CA, USA).

    Techniques:

    Comparison of ERG, CD31, and D2-40 endothelial markers. (A) ERG, panendothelial marker showing nuclear immunoreactivity in artery, vein, and lymphatics. (B) ERG immunostaining specific for endothelial cells without cross-reactivity. (C) D31 immunostaining showing cross-reactivity in inflammatory cells. (D) D2-40 immunostaining showing cross-reactivity in fibroblasts.

    Journal: Korean Journal of Pathology

    Article Title: ERG Immunohistochemistry as an Endothelial Marker for Assessing Lymphovascular Invasion

    doi: 10.4132/KoreanJPathol.2013.47.4.355

    Figure Lengend Snippet: Comparison of ERG, CD31, and D2-40 endothelial markers. (A) ERG, panendothelial marker showing nuclear immunoreactivity in artery, vein, and lymphatics. (B) ERG immunostaining specific for endothelial cells without cross-reactivity. (C) D31 immunostaining showing cross-reactivity in inflammatory cells. (D) D2-40 immunostaining showing cross-reactivity in fibroblasts.

    Article Snippet: Primary antibodies were CD31 (1:25, Thermo Fisher Scientific Inc., Kalamazoo, MI, USA), D2-40 (predilution, Dako, Glostrup, Denmark), and ERG (predilution, Biocare Medical, Concord, CA, USA).

    Techniques: Marker, Immunostaining

    Chemoattractants stimulate release of TNF from neutrophils in vitro and in vivo. Mixed mouse blood leukocytes were treated with PBS (control) or stimulated with LTB 4 (10 or 30 min). Supernatants were assayed for soluble TNF by ELISA and cells were permeabilized and immunostained for analysis of intracellular TNF by flow cytometry and confocal microscopy. (A) Representative flow cytometry histograms from 4 independent experiments showing the binding of anti-TNF mAb (black lines) or control IgG (filled). (B) Quantification of intracellular TNF by flow cytometry (expressed as RFI; n = 6 blood samples for PBS and 30 min LTB 4 , n = 5 for 10 min LTB 4 ) from 4 independent experiments. (C) Quantification of released TNF ( n = 4) from 4 independent experiments. ND, not detected. (D) Representative confocal images of neutrophils from two independent experiments show cells treated with PBS or LTB 4 (10 and 30 min) and stained for the neutrophil marker MRP-14 (green) or TNF (red). Bar, 5 µm. (E) Representative 3D-reconstructed images of LTB 4 -stimulated cremasteric postcapillary venule (luminal side) showing GFP-neutrophils and PECAM-1–labeled ECs (red). The top panel shows neutrophils at different steps of the transmigration response, i.e., luminal crawling, preTEM phase (6 min before breaching ECs), TEM phase, and abluminal crawling. The associated TNF detected on the leukocyte surface for each step (intensity rainbow color code from blue [low intensity] to red [high intensity]) is shown in the bottom panels with and without the associated neutrophil. Bar, 5 µm. (F) Mean fluorescent intensity of signals on neutrophils was quantified in mice injected with anti-TNF or control mAbs ( n = 4 mice/group) from 4 independent experiments. A total of ∼40 neutrophils were tracked and analyzed for each group. All data are means ± SEM. Statistical differences from PBS (B and C), signals from luminal crawling cells (F), or other comparisons (indicated by lines) are shown by asterisks. *, P

    Journal: The Journal of Experimental Medicine

    Article Title: Neutrophils recruited by chemoattractants in vivo induce microvascular plasma protein leakage through secretion of TNF

    doi: 10.1084/jem.20132413

    Figure Lengend Snippet: Chemoattractants stimulate release of TNF from neutrophils in vitro and in vivo. Mixed mouse blood leukocytes were treated with PBS (control) or stimulated with LTB 4 (10 or 30 min). Supernatants were assayed for soluble TNF by ELISA and cells were permeabilized and immunostained for analysis of intracellular TNF by flow cytometry and confocal microscopy. (A) Representative flow cytometry histograms from 4 independent experiments showing the binding of anti-TNF mAb (black lines) or control IgG (filled). (B) Quantification of intracellular TNF by flow cytometry (expressed as RFI; n = 6 blood samples for PBS and 30 min LTB 4 , n = 5 for 10 min LTB 4 ) from 4 independent experiments. (C) Quantification of released TNF ( n = 4) from 4 independent experiments. ND, not detected. (D) Representative confocal images of neutrophils from two independent experiments show cells treated with PBS or LTB 4 (10 and 30 min) and stained for the neutrophil marker MRP-14 (green) or TNF (red). Bar, 5 µm. (E) Representative 3D-reconstructed images of LTB 4 -stimulated cremasteric postcapillary venule (luminal side) showing GFP-neutrophils and PECAM-1–labeled ECs (red). The top panel shows neutrophils at different steps of the transmigration response, i.e., luminal crawling, preTEM phase (6 min before breaching ECs), TEM phase, and abluminal crawling. The associated TNF detected on the leukocyte surface for each step (intensity rainbow color code from blue [low intensity] to red [high intensity]) is shown in the bottom panels with and without the associated neutrophil. Bar, 5 µm. (F) Mean fluorescent intensity of signals on neutrophils was quantified in mice injected with anti-TNF or control mAbs ( n = 4 mice/group) from 4 independent experiments. A total of ∼40 neutrophils were tracked and analyzed for each group. All data are means ± SEM. Statistical differences from PBS (B and C), signals from luminal crawling cells (F), or other comparisons (indicated by lines) are shown by asterisks. *, P

    Article Snippet: Labeling of ECs was performed by intrascrotal injection of a nonblocking anti–PECAM-1 mAb conjugated with Alexa Fluor 555 (C390; eBioscience; 2 µg/mouse) at least 2 h before the exteriorization of the cremaster muscle.

    Techniques: In Vitro, In Vivo, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Cytometry, Confocal Microscopy, Binding Assay, Staining, Marker, Labeling, Transmigration Assay, Transmission Electron Microscopy, Mouse Assay, Injection

    Optical coherence tomography of MPIO on a cell monolayer. (A) A cartoon representation of antibody-labelled MPIO [red] binding to endothelial cell surface markers [yellow]. The PECAM-1–MPIO bound to the cell monolayer are visible as a bright horizontal band in the OCT image (B). ‘No-MPIO’ control experiment confirms background signal is minimal (C). The intensity profile of a line drawn perpendicular to the monolayer with PECAM-1–MPIO bound reveals a clear demarcation between MPIO and surrounding agarose and cells (D). Areas of measurable signal along the pullback are significantly greater for PECAM-1–MPIO compared with the no MPIO control (E) (Error bars represent ±1 SEM). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

    Journal: Atherosclerosis

    Article Title: Molecular imaging with optical coherence tomography using ligand-conjugated microparticles that detect activated endothelial cells: Rational design through target quantification

    doi: 10.1016/j.atherosclerosis.2011.07.127

    Figure Lengend Snippet: Optical coherence tomography of MPIO on a cell monolayer. (A) A cartoon representation of antibody-labelled MPIO [red] binding to endothelial cell surface markers [yellow]. The PECAM-1–MPIO bound to the cell monolayer are visible as a bright horizontal band in the OCT image (B). ‘No-MPIO’ control experiment confirms background signal is minimal (C). The intensity profile of a line drawn perpendicular to the monolayer with PECAM-1–MPIO bound reveals a clear demarcation between MPIO and surrounding agarose and cells (D). Areas of measurable signal along the pullback are significantly greater for PECAM-1–MPIO compared with the no MPIO control (E) (Error bars represent ±1 SEM). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

    Article Snippet: Antibodies to human VCAM-1, E-selectin and PECAM-1 were incubated with cells at 4 °C overnight (final concentration 20 μg mL−1 ) and, after washing, incubated with goat anti-mouse Alexa Fluor 488 (Invitrogen) (5 μg mL−1 ) for 30 min at 37 °C.

    Techniques: Binding Assay

    OCT imaging of MPIO binding to E-selectin and VCAM-1 under conditions of shear stress. Binding of E + V–MPIO at 1 dyne cm −2 was detectable using OCT, and the particles bound to the cell monolayer were clearly visible (A). No signal was seen in the basal control at 1 dyne cm −2 (B). The intensity profile of a line drawn perpendicular to the monolayer with PECAM-1–MPIO bound reveals a clear demarcation between MPIO and surrounding agarose and cells (C). Area of signal generated by the E + V–MPIO binding at 1 dyne cm −2 in the OCT images is significantly higher in the stimulated cells than in the basal controls (D E), while the reduction in binding to stimulated cells at 5 dyne cm −2 results in a lower signal area, but which is still significantly greater than the basal equivalent (E). Error bars represent ±1 SEM.

    Journal: Atherosclerosis

    Article Title: Molecular imaging with optical coherence tomography using ligand-conjugated microparticles that detect activated endothelial cells: Rational design through target quantification

    doi: 10.1016/j.atherosclerosis.2011.07.127

    Figure Lengend Snippet: OCT imaging of MPIO binding to E-selectin and VCAM-1 under conditions of shear stress. Binding of E + V–MPIO at 1 dyne cm −2 was detectable using OCT, and the particles bound to the cell monolayer were clearly visible (A). No signal was seen in the basal control at 1 dyne cm −2 (B). The intensity profile of a line drawn perpendicular to the monolayer with PECAM-1–MPIO bound reveals a clear demarcation between MPIO and surrounding agarose and cells (C). Area of signal generated by the E + V–MPIO binding at 1 dyne cm −2 in the OCT images is significantly higher in the stimulated cells than in the basal controls (D E), while the reduction in binding to stimulated cells at 5 dyne cm −2 results in a lower signal area, but which is still significantly greater than the basal equivalent (E). Error bars represent ±1 SEM.

    Article Snippet: Antibodies to human VCAM-1, E-selectin and PECAM-1 were incubated with cells at 4 °C overnight (final concentration 20 μg mL−1 ) and, after washing, incubated with goat anti-mouse Alexa Fluor 488 (Invitrogen) (5 μg mL−1 ) for 30 min at 37 °C.

    Techniques: Imaging, Binding Assay, Generated

    Binding of E-selectin-, VCAM-1-, E + V-, PECAM-1- and IgG 2 –MPIO to TNF-α stimulated and basal HUVEC. In stimulated cells under static and low shear stress conditions, antibody–MPIO to E-selectin, VCAM-1 and E + V bind in greater numbers than PECAM-1–MPIO. However, as shear stress increases, PECAM-1–MPIO bind in significantly greater numbers than the other antibody–MPIO (A). In basal cells, only antibody–MPIO targeted to the constitutively expressed PECAM-1 are able to bind above background (B). Data points are expressed as mean MPIO bound per field of view (MPIO/fov), with error bars representing ±1 SEM.

    Journal: Atherosclerosis

    Article Title: Molecular imaging with optical coherence tomography using ligand-conjugated microparticles that detect activated endothelial cells: Rational design through target quantification

    doi: 10.1016/j.atherosclerosis.2011.07.127

    Figure Lengend Snippet: Binding of E-selectin-, VCAM-1-, E + V-, PECAM-1- and IgG 2 –MPIO to TNF-α stimulated and basal HUVEC. In stimulated cells under static and low shear stress conditions, antibody–MPIO to E-selectin, VCAM-1 and E + V bind in greater numbers than PECAM-1–MPIO. However, as shear stress increases, PECAM-1–MPIO bind in significantly greater numbers than the other antibody–MPIO (A). In basal cells, only antibody–MPIO targeted to the constitutively expressed PECAM-1 are able to bind above background (B). Data points are expressed as mean MPIO bound per field of view (MPIO/fov), with error bars representing ±1 SEM.

    Article Snippet: Antibodies to human VCAM-1, E-selectin and PECAM-1 were incubated with cells at 4 °C overnight (final concentration 20 μg mL−1 ) and, after washing, incubated with goat anti-mouse Alexa Fluor 488 (Invitrogen) (5 μg mL−1 ) for 30 min at 37 °C.

    Techniques: Binding Assay

    FISH analysis in human RCC and normal renal tissue sections. A: CA IX immunostaining in RCC tissue and normal kidney tissue. Upper panels show CD31 staining in vascular ECs. Lower panels show that CA IX was expressed in tumor cells in RCC tissue but not

    Journal: The American Journal of Pathology

    Article Title: Cytogenetic Abnormalities of Tumor-Associated Endothelial Cells in Human Malignant Tumors

    doi: 10.2353/ajpath.2009.090202

    Figure Lengend Snippet: FISH analysis in human RCC and normal renal tissue sections. A: CA IX immunostaining in RCC tissue and normal kidney tissue. Upper panels show CD31 staining in vascular ECs. Lower panels show that CA IX was expressed in tumor cells in RCC tissue but not

    Article Snippet: The cells were then incubated with anti-human CD31 antibody (eBioscience, San Diego, CA), and hTECs or hNECs were isolated by MACS according to the manufacturer’s instructions, using anti-mouse IgG microbeads (Miltenyi Biotec).

    Techniques: Fluorescence In Situ Hybridization, Immunostaining, Staining

    FISH analysis in freshly isolated and cytospun hTECs and hNECs. A and B: FISH analysis of freshly isolated and cytospun hTECs and hNECs. hTECs ( A ) and hNECs ( B ) were stained for CD31, VE-cadherin, or the RCC marker CA IX. FISH was performed using chromosome

    Journal: The American Journal of Pathology

    Article Title: Cytogenetic Abnormalities of Tumor-Associated Endothelial Cells in Human Malignant Tumors

    doi: 10.2353/ajpath.2009.090202

    Figure Lengend Snippet: FISH analysis in freshly isolated and cytospun hTECs and hNECs. A and B: FISH analysis of freshly isolated and cytospun hTECs and hNECs. hTECs ( A ) and hNECs ( B ) were stained for CD31, VE-cadherin, or the RCC marker CA IX. FISH was performed using chromosome

    Article Snippet: The cells were then incubated with anti-human CD31 antibody (eBioscience, San Diego, CA), and hTECs or hNECs were isolated by MACS according to the manufacturer’s instructions, using anti-mouse IgG microbeads (Miltenyi Biotec).

    Techniques: Fluorescence In Situ Hybridization, Isolation, Staining, Marker

    FISH analysis in uncultured and cultured mTECs and mNECs. mTECs isolated from xenografts of human epithelial tumors were aneuploid. Cultured and uncultured mTECs were positive for CD31 (green). Nuclei were counterstained with DAPI (blue). Three or more

    Journal: The American Journal of Pathology

    Article Title: Cytogenetic Abnormalities of Tumor-Associated Endothelial Cells in Human Malignant Tumors

    doi: 10.2353/ajpath.2009.090202

    Figure Lengend Snippet: FISH analysis in uncultured and cultured mTECs and mNECs. mTECs isolated from xenografts of human epithelial tumors were aneuploid. Cultured and uncultured mTECs were positive for CD31 (green). Nuclei were counterstained with DAPI (blue). Three or more

    Article Snippet: The cells were then incubated with anti-human CD31 antibody (eBioscience, San Diego, CA), and hTECs or hNECs were isolated by MACS according to the manufacturer’s instructions, using anti-mouse IgG microbeads (Miltenyi Biotec).

    Techniques: Fluorescence In Situ Hybridization, Cell Culture, Isolation