Increased stability of Bcl-2 in HSP70-mediated protection against apoptosis induced by oxidative stress

被引：77

作者：

Jiang, Bimei ^{[1
]}

Liang, Pengfei ^{[2
]}

Deng, Gonghua ^{[1
]}

Tu, Zizhi ^{[1
]}

Liu, Meidong ^{[1
]}

Xiao, Xianzhong ^{[1
]}

机构：

[1] Cent S Univ, Xiangya Sch Med, Dept Pathophysiol, Changsha 410008, Hunan, Peoples R China

[2] Cent S Univ, Xiangya Hosp, Dept Burns & Plast Surg, Changsha 410008, Hunan, Peoples R China

来源：

CELL STRESS & CHAPERONES | 2011年 / 16卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Apoptosis; Heat shock protein 70; Hydrogen peroxide; Smac; Bcl-2; C2C12 myogenic cells; C2C12 MYOGENIC CELLS; HEAT-SHOCK; CYTOCHROME-C; MEDIATED APOPTOSIS; HYDROGEN-PEROXIDE; DEATH; HEAT-SHOCK-PROTEIN-70; PROTEINS; HSP70; RELEASE;

D O I：

10.1007/s12192-010-0226-6

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

We have previously shown that heat shock protein 70 (HSP70) markedly inhibits H2O2-induced apoptosis in mouse C2C12 myogenic cells by reducing the release of Smac. However, the molecular mechanism by which HSP70 interferes with Smac release during oxidative stress-induced apoptosis is not understood. In the current study, we showed that HSP70 increased the stability of Bcl-2 during oxidative stress. An antisense phosphorothioate oligonucleotide against Bcl-2 caused selective inhibition of Bcl-2 protein expression induced by HSP70 and significantly attenuated HSP70-mediated cell protection against H2O2-induced release of Smac and apoptosis. Taken together, our results indicate that there are important relationships among HSP70, Bcl-2, release of Smac, and induction of apoptosis by oxidative stress.

引用

页码：143 / 152

页数：10

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