Angiopoietin-1 protects H9c2 cells from H2O2-induced apoptosis through AKT signaling
Angiopoietin-1 protects H9c2 cells from H2O2-induced apoptosis through AKT signaling
复制标题
Angiopoietin-1 通过 AKT 信号传导保护 H9c2 细胞免受 H2O2 诱导的细胞凋亡
DOI：
10.1016/j.bbrc.2007.05.172
复制
发表时间：
2007-08-03
影响因子：
3.1
通讯作者：
Zhou Chunyan
中科院分区：
文献类型：
--
作者：
Wang Zuoyan;Cui Ming;Zhou Chunyan
心肌细胞凋亡导致的心肌细胞损失被认为是导致心室重构和心力衰竭的原因。活性氧诱导的心肌细胞凋亡在心脏的多种病理过程中起重要作用。本研究采用过氧化氢（H2 O2）处理培养的H9 c2心肌细胞，观察血管生成素-1（Ang 1）对心肌细胞抗氧化应激的直接保护作用。流式细胞术、TUNEL法和DNA梯状电泳检测细胞凋亡。H2 O2处理引起H9 c2细胞典型的凋亡，并呈时间依赖性。转染表达Ang 1的重组腺病毒后，H9 c2细胞中AKT蛋白持续磷酸化，H2 O2诱导的细胞凋亡受到抑制。这些结果表明，Ang 1通过调节AKT的活性来保护心肌细胞免受氧化应激诱导的凋亡。All rights reserved.
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.