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p62 prevents carbonyl cyanide m-chlorophenyl hydrazine (CCCP)-induced apoptotic cell death by activating Nrf2

Title
p62 prevents carbonyl cyanide m-chlorophenyl hydrazine (CCCP)-induced apoptotic cell death by activating Nrf2
Authors
Park, Jeong SuKang, Dong HoonBae, Soo Han
Ewha Authors
강동훈
SCOPUS Author ID
강동훈scopus
Issue Date
2015
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN
0006-291XJCR Link1090-2104JCR Link
Citation
vol. 464, no. 4, pp. 1139 - 1144
Keywords
CCCPp62AutophagyNrf2Keap1
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Carbonyl cyanide m-chlorophenyl hydrazone (CCCP) is a mitochondrial depolarizing agent that induces reactive oxygen species (ROS)-mediated cell death. The Nrf2-Keap1 pathway is crucial for the elimination of ROS in stressed cells. However, the molecular mechanism underlying the regulation of the Nrf2-Keap1 pathway in CCCP-induced cell death is unknown. In this study, we demonstrated that CCCP promotes Keap1 degradation, and thereby activates Nrf2. This CCCP-mediated Keap1 degradation is partly dependent on autophagy. Moreover, CCCP-induced Keap1 degradation is mainly reliant on p62, which functions as an adaptor protein during selective autophagy. Lack of p62 blocked CCCP-induced Keap1 degradation and inhibited Nrf2 activation, and thereby increased the accumulation of ROS. Ablation of p62 increased the susceptibility of cells to oxidative stress. These results indicate that p62 plays an important role in protecting cells against oxidative stress through Keap1 degradation-mediated Nrf2 activation. (C) 2015 Elsevier Inc. All rights reserved.
DOI
10.1016/j.bbrc.2015.07.093
Appears in Collections:
연구기관 > 세포항상성연구센터 > Journal papers
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