Angiopoietin-1 protects H9c2 cells from H2O2-induced apoptosis through AKT signaling

被引：31

作者：

Wang Zuoyan

Cui Ming

Sun Lijie

Jia Zhuqing

Bai Yun

Ma Kangtao

Chen Fengrong ^{[1
]}

Zhou Chunyan

机构：

[1] Peking Univ Third Hosp, Dept Cardiol, Beijing 100083, Peoples R China

[2] Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Sch Basic Med Sci, Beijing 100083, Peoples R China

[3] Peking Univ, Hlth Sci Ctr, Dept Cell Biol, Sch Basic Med Sci, Beijing 100083, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 359卷 / 03期

基金：

中国国家自然科学基金; 新加坡国家研究基金会;

关键词：

angiopoietin-1; oxidative stress; myocyte apoptosis; AKT;

D O I：

10.1016/j.bbrc.2007.05.172

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Loss of cardiomyocytes by apoptosis is proposed to cause ventricular remodeling and heart failure. Reactive oxygen species-induced apoptosis of cardiomyocytes has been reported to play an important role in many types of pathological processes of the heart. We investigated whether angiopoietin-1 (Ang1) has direct cytoprotective effects on cardiomyocytes against oxidative stress. Cultured H9c2 cells (cardiomyocytes) were treated with hydrogen peroxide (H2O2). Apoptosis was evaluated by flow cytometry, TUNEL assay and DNA laddering. The H2O2 treatment caused typical apoptosis of H9c2 cells in a time-dependent manner. Transfection of recombinant adenovirus expressing Ang1 resulted in a sustained phosphorylation of AKT and inhibition Of H2O2-induced apoptosis in H9c2 cells. This effect could be reversed by AKT inhibition. These results suggest that Ang1 protects cardiomyocytes from oxidative stress-induced apoptosis by regulating the activity of AKT, (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：685 / 690

页数：6

共 12 条

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