NDLI: Heat shock transcription factor-1 inhibits H$_{2}$O$_{2}$-induced apoptosis via down-regulation of reactive oxygen species in cardiac myocytes

Content Provider	Springer Nature Link
Author	Zhang, Lei Jiang, Hong Gao, Xiaoqing Zou, Yunzeng Liu, Ming Liang, Yanyan Yu, Ying Zhu, Weidong Chen, Haozhu Ge, Junbo
Copyright Year	2010
Abstract	Heat shock transcription factor-1 (HSF1) protects against cardiac diseases such as ischemia/reperfusion injury and myocardial infarction. However, the mechanisms have not yet been fully characterized. In this study, we investigated the effects of reactive oxygen species (ROS) and apoptosis signal-regulating kinase-1 (ASK1) in HSF1-regulated cardiomyocyte protection. Cultured cardiomyocytes of neonatal rats were transfected with HSF1, ASK1 or both of them before exposure to H$_{2}$O$_{2}$, and the ROS generation, c-Jun N-terminal kinase (JNK) activity and apoptosis were examined. H$_{2}$O$_{2}$ significantly increased intracellular ROS generation and apoptotic cells as expected, and all these cellular events were greatly inhibited by overexpression of HSF1. However, H$_{2}$O$_{2}$-induced increases in JNK phosphorylation and cell apoptosis were largely enhanced by ASK1 overexpression whereas the similar transfection did not affect the ROS generation in the cells. Moreover, inhibition of H$_{2}$O$_{2}$-increased ROS generation, JNK phosphorylation, and cellular apoptosis by overexpression of HSF1 tended to be disappeared, when the cells were co-transfected with ASK1. These results suggest that HSF1 protects cardiomyocytes from apoptosis under oxidative stress via down-regulation of intracellular ROS generation and inhibition of JNK phosphorylation. Although ASK1 itself has no effect on intracellular ROS generation, it may affect the inhibitory effects of HSF1 on ROS generation, JNK activity, and cardiomyocyte injury.
Starting Page	21
Ending Page	28
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	347
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2010-10-13
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Heat shock transcription factor-1 Cardiomyocytes Reactive oxygen species Apoptosis signal-regulating kinase-1 c-Jun N-terminal kinase Cardiology Oncology Medical Biochemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

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