Paxillin regulates vascular endothelial growth factor A-induced in vitro angiogenesis of human umbilical vein endothelial cells

被引:18
|
作者
Yang, Wan-Ju [1 ,2 ]
Yang, Yan-Ning [1 ]
Cao, Jin [1 ]
Man, Zi-Hui [1 ]
Li, Ying [1 ]
Xing, Yi-Qiao [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Ctr Eye, Wuhan 430060, Hubei, Peoples R China
[2] Huazhong Univ Sci & Technol, Cent Hosp Wuhan, Dept Ophthalmol, Tongji Med Coll, Wuhan 430014, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
paxillin; vascular endothelial growth factor; endothelium; angiogenesis; CORNEAL EPITHELIAL-CELLS; FOCAL ADHESION KINASE; NEOVASCULARIZATION; VEGF; PHOSPHORYLATION; ACTIVATION; MIGRATION; EXPRESSION; CANCER; VIRUS;
D O I
10.3892/mmr.2014.2961
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The purpose of the present study was to investigate the role of paxillin in the vascular endothelial growth factor A (VEGF-A)-induced adhesion, proliferation, migration and capillary formation of endothelial cells (ECs) in vitro. Human umbilical vein ECs (HUVECs) were used to evaluate these four processes in vitro. The HUVECs were either mock-transfected (control), transfected with scramble small interference RNA (siRNA) or transfected with siRNA specifically targeting paxillin. VEGF-A (20 ng/ml) was used to stimulate angiogenesis. The VEGF-A treatment significantly increased the adhesion, proliferation, migration and tube formation of the HUVECs in the control and scramble siRNA groups, whereas the siRNA-mediated knockdown of paxillin inhibited these VEGF-A-induced effects. Paxillin is essential for VEGF-A-mediated angiogenesis in ECs and its inhibition may be a potential target for antiangiogenic therapies.
引用
收藏
页码:1784 / 1792
页数:9
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