期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 481, 期 1-2, 页码 125-131出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.10.153
关键词
Hsp60; Outer mitochondrial membrane; Apoptosis; Bax; Mitochondrial permeability transition pore; Mitochondrial ROS
资金
- National Key Basic Research Program of China (973 Program) [2014CB138502]
- National Natural Science Foundation of China [31602027, 31672520]
- China Postdoctoral Science Foundation [2016M591860]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Graduate Research and Innovation Projects in Jiangsu Province
- Sino-German Agricultural Cooperation Project of the Federal Ministry of Food, Agriculture and Consumer Production, Berlin, Germany
- Jiangsu Natural Science Foundation of China [BK20160732]
Hsp60 is a typical mitochondrial protein in eukaryotes, and is involved in facilitating the correction of misfolded protein back into the correct conformation. Previous, we identified aspirin-induced HSPs in response to heat stress [1]. To investigate whether Hsp60 can protect against death under heat stress, we used lenti-siRNA to knock down the expression of Hsp60. When exposed to heat stress, more apoptosis was observed with increasing exposure to heat stress, while necrosis was not affected. Furthermore, heat stress induced the loss of mitochondrial membrane potential (Delta psi m) and a significant increase of reactive oxygen species (ROS) produced in mitochondria as measured by TMRE and MitoSOXTM red. The loss of Delta psi m indicated a change in inner mitochondrial function. Real-time Quantitative PCR was used to investigate the mechanism by detecting mRNA expression profile of the inner mitochondrial membrane, including CypD, ANT, and PIC. Results showed no differences between lenti-siRNA Hsp60 and control. However, bax in the cytoplasm translocated to mitochondrial during heat stress and regulated the permeability of outer mitochondrial membrane. We hypothesize that Hsp60 can protect cardiac myocytes against apoptosis involving in outer mitochondrial membrane not the inner mitochondrial membrane under heat stress. (C) 2016 Elsevier Inc. All rights reserved.
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