Objective To explore the effect and mechanism of vascular endothelial cadherin （VE-cadherin） on the development of experimental corneal neovascularization. Methods This was an animal experimental study. Mouse corneas were burned by NaOH to induce corneal neovascularization. The gene expression of VE-cadherin in burned corneas was examined by RT-PCR. The neutralizing anti-VE-cadherin antibody was locally administrated 1 week after the alkali injury and the formation of corneal neovascularization was examined 3 weeks after the injury by corneal whole mount staining with CD31. The mRNA expression of caspase-3 in burned corneas was detected by RT-PCR and the number of apoptosis neovascular endothelial cells in corneas was examined by FCS （flow cytometry）. The effect of VE-cadherin on human retinal endothelial cells （HRECs） tube formation was detected in vitro. Data were analyzed statistically with a two-tailed Student′s t-test. Results Compared to the control group， the group treated with the neutralizing anti-VE-cadherin antibody showed significantly decreased corneal neovascularization. RT-PCR confirmed that neutralizing anti-VE-cadherin antibody treatment resulted in an increase of caspase-3 expression in corneal tissue. FCS revealed that antibody treatment resulted in increased intracorneal apoptosis neovascular endothelial cells. In addition， the tube formation ability of HRECs was found to be significantly inhibited by neutralizing antibody in vitro. Conclusion VE-cadherin plays vital roles in experimental corneal neovascularization by down-regulating caspase-3 mRNA expression， reducing the number of apoptic cells and promoting cell-cell adhesion.
刘高勤,陈磊,肖艳辉,陈志刚,陆培荣. 血管内皮钙黏蛋白对实验性角膜新生血管的作用及机制[J]. 中华眼视光学与视觉科学杂志, 2013, 15(3): 174-177.
LIU Gao-qin,CHEN Lei,XIAO Yan-hui,CHEN Zhi-gang,LU Pei-rong. The effect and mechanism of VE-cadherin on the development of experimental corneal neovascularization. Chinese Journal of Optometry Ophthalmology and Visual Science, 2013, 15(3): 174-177. DOI: 10.3760/cma.j.issn.1674-845X.2013.03.011
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