SIRT4 Prevents Hypoxia-Induced Apoptosis in H9c2 Cardiomyoblast Cells

被引：100

作者：

Liu, Ban ^{[1
]}

Che, Wenliang ^{[1
]}

Xue, Jinsong ^{[2
]}

Zheng, Changzhu ^{[3
]}

Tang, Kai ^{[1
]}

Zhang, Jingying ^{[1
]}

Wen, Jing ^{[1
]}

Xu, Yawei ^{[1
]}

机构：

[1] Tongji Univ, Sch Med, Dept Cardiol, Shanghai Peoples Hosp 10, Shanghai 200072, Peoples R China

[2] Nanjing Med Univ, Eye Hosp, Nanjing 210029, Jiangsu, Peoples R China

[3] Pudong New Area Zhoupu Hosp, Dept Cardiol, Shanghai 201318, Peoples R China

来源：

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY | 2013年 / 32卷 / 03期

基金：

中国国家自然科学基金;

关键词：

SIRT4; Hypoxia; Apoptosis; Cardiomyoblast; BCL-2; FAMILY-MEMBERS; MITOCHONDRIA; ACTIVATION; CASPASES; DEATH;

D O I：

10.1159/000354469

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Aims: Apoptosis plays a critical role in cardiomyocyte loss during ischaemic heart injury. A detailed understanding of the mechanism involved has a substantial impact on the optimization and development of treatment strategies. Here, we report that the expression of SIRT4, a mitochondrial sirtuin, is markedly down-regulated in hypoxia-induced apoptosis of H9c2 cardiomyoblast cells. Methods and Results: SIRT4 interference significantly alters H9c2 cell viability, apoptotic cell number and caspase-3/7 activity. Furthermore, SIRT4 expression can affect the ratio of pro-caspase 9/caspase 9 or pro-caspase 3/caspase 3, an affect Bax translocation, which in turn alters the development of H9c2 cell apoptosis. Conclusion: These results suggest that SIRT4 is a key player in hypoxia-induced cardiomyocyte apoptosis, and that strategies based on its enhancement might be of benefit in the treatment of ischaemic heart disease. Copyright (C) 2013 S. Karger AG, Basel

引用

页码：655 / 662

页数：8

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