Angiopoietin-1 Protects the Endothelial Cells Against Advanced Glycation End Product Injury by Strengthening Cell Junctions and Inhibiting Cell Apoptosis

作者：Zhao, Jingling; Chen, Lei; Shu, Bin; Tang, Jinming; Zhang, Lijun; Xie, Julin; Liu, Xusheng; Xu, Yingbin; Qi, Shaohai^*

来源：Journal of Cellular Physiology, 2015, 230(8): 1895-1905.

DOI：10.1002/jcp.24920

• BLOOD-RETINAL BARRIER
• GROWTH-FACTOR
• TYROSINE PHOSPHORYLATION
• TIE2 RECEPTOR
• IN-VITRO
• EXPRESSION
• SURVIVAL
• ANGIOGENESIS
• DISRUPTION
• ACTIVATION

Endothelial dysfunction is a major characteristic of diabetic vasculopathy. Protection of the vascular endothelium is an essential aspect of preventing and treating diabetic vascular complications. Although Angiopoietin-1 (Ang-1) is an important endothelial-specific protective factor, whether Ang-1 protects vascular cells undergoing advanced glycation end product (AGE) injury has not been investigated. The aim of the present study was to determine the potential effects of Ang-1 on endothelial cells after exposure to AGE. We show here that Ang-1 prevented AGE-induced vascular leakage by enhancing the adherens junctions between endothelial cells, and this process was mediated by the phosphorylation and membrane localization of VE-cadherin. Furthermore, Ang-1 also protected endothelial cells from AGE-induced death by regulating phosphatidylinositol 3-kinase (PI3K)/Akt-dependent Bad phosphorylation. Our findings suggest that the novel protective mechanisms of Ang-1 on endothelium are achieved by strengthening endothelial cell junctions and reducing endothelial cell death after AGE injury. J. Cell. Physiol. 230: 1895-1905, 2015.

• 出版日期2015-8
• 单位中山大学