期刊
CELL STRESS & CHAPERONES
卷 16, 期 2, 页码 143-152出版社
SPRINGER
DOI: 10.1007/s12192-010-0226-6
关键词
Apoptosis; Heat shock protein 70; Hydrogen peroxide; Smac; Bcl-2; C2C12 myogenic cells
类别
资金
- National Basic Research Program of China [2007CB512007]
- National Natural Science Foundation of China [30700290]
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据