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Anti-apoptosis effects of vascular endothelial cadherin in experimental corneal neovascularization

International Journal of Ophthalmology(English edition) 2015年第6期8卷 1083-1088页

作者： Gao-Qin Liu Hong-Ya Wu Jing Xu Meng-Jiao Wang Pei-Rong Lu Xue-Guang Zhang Department of Ophthalmology the First Affiliated Hospital of Soochow University Jiangsu Clinical Immunology Institute the First Affiliated Hospital of Soochow University

AIMTo explore the effects and mechanism of vascular endothelial cadherin (VE-cadherin) on experimental corneal neovascularization (CRNV).METHODSMouse corneas were burned with sodium hydroxide to build a CRNV model. The burned corneas were locally administrated with anti-mouse VE-cadherin neutralizing antibody. Annexin V and cluster of differentiation 31 (CD31) double staining was used to measure vascular endothelial cell apoptosis with the use of flow cytometry (FCM). The protein expression of NADPH oxidase 2 (Nox2), caspase-3, and protein kinase C (PKC) in the burned corneas were examined by Western blot. Human retinal endothelial cell (HREC) proliferation was detected using a Cell Counting Kit 8 (CCK-8) assay in *** amount of CRNV peaked two weeks after the alkali burn. FCM confirmed that VE-cadherin neutralizing antibody treatment increased CD31 positive cell apoptosis. Western blot revealed that the intracorneal protein expression of Nox2 and caspase-3 were up-regulated, while PKC was down-regulated in the VE-cadherin neutralizing antibody administrated group. CCK-8 assay showed that VE-cadherin neutralizing antibody markedly inhibited HREC ***-cadherin exhibited an anti-apoptosis effect through enhanced PKC signaling and an enhanced cell proliferation pathway.

关键词： vascular endothelial cadherin neovascularization cornea chemokine

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Sprouty4 regulated vascular permeability by regulating the tyrosine phosphorylation and degradation of VE-cadherin

Sprouty4 regulated vascular permeability by regulating the t...

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中国生物化学与分子生物学会2019年全国学术会议暨学会...

作者： Jiangbo Ren Nannan Zhang Wenjie Sun Yuan Luo Yuke Gao Yan Gong Department of Biological Repositories Zhongnan Hospital of Wuhan University Department of Radiation and Medical Oncology Zhongnan Hospital of Wuhan University

Regulation of endothelial cell adherent junctions is important to pathophysiological processes, in which vascular integrity is disrupted such as during tumor angiogenesis and chronic inflammatory conditions. The effects of Sprouty4(Spry4) on endothelial barrier function was investigated using vascular endothelial cell growth factor(VEGF)-induced vascular permeability model. In the present study we showed that overexpression of Spry4 inhibited vascular permeability in primary human endothelial cells in vitro and in Spry4-expressing transgenic mice in vivo. Conversely, knockdown of Spry4 in vitro and conditional endothelial cell-specific knockout of Spry4 in endothelial cells in vivo enhanced VEGF-induced vascular permeability. In addition, overexpression of Spry4 inhibited VEGF-induced vascular endothelial cadherin(VE-cadherin) tyrosine phosphorylation, in part by inhibiting c-Src activation, and resistance to VEGF-induced vascular permeability. Inhibition of VEGF-induced VE-cadherin tyrosine phosphorylation and decreased vascular permeability by Spry4 overexpression could be rescued by expression of constitutively active c-Src. Conversely, knockdown of Spry4 in endothelial cells increased tyrosine phosphorylation of VE-cadherin and vascular permeability, which was repressed by dominant negative Src(DNSrc). Consistent with these results, DNSrc repressed the increase in vascular permeability that resulted due to knockdown of Spry4. Taken together, these results suggested that Spry4 regulated vascular permeability via regulating the activation of c-Src by VEGF signaling and consequently the tyrosine phosphorylation of VE-cadherin.

关键词： vascular integrity endothelial permeability vascular endothelial growth factor receptor 2 vascular endothelial cadherin Sprouty

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