Document Detail


Hes1 is upregulated by ischemic postconditioning and contributes to cardioprotection.
MedLine Citation:
PMID:  25431316     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The expression of Hes1 is increased following myocardial infarct and other ischemic cardiomyopathies, but the role of Hes1 in cardioprotection provided by ischemic postconditioning (IPost) remains unclear. In this study, we used gain and loss of function approaches to investigate the role of Hes1 in cardioprotection during IPost. Primary cardiac myocytes exposed to ischemia reperfusion injury (IRI) and IPost were used as the experimental model. The results showed that Hes1 expression was increased during myocardial IPost, and Hes1 promoted the viability while inhibited the apoptosis of cardiomyocytes. Moreover, Hes1 inhibited the opening of mitochondrial permeability transition pore (mPTP) and the generation of reactive oxygen species in primary cardiac myocytes exposed to IRI. Mechanistically, we found that Hes1-mediated cardioprotection was related to the downregulation of phosphatase and tensin homolog and the activation of phosphatidylinositol 3-kinase/Akt and signal transducer and activator of transcription 3 signalling. These data demonstrate that Hes1 is upregulated and mediates cardioprotection provided by IPost and suggest that Hes1 is a potential new target for the treatment of ischemic cardiomyopathy. Copyright © 2014 John Wiley & Sons, Ltd.
Authors:
Xue-Liang Zhou; Yong Zhao; Yi-Hu Fang; Qi-Rong Xu; Ji-Chun Liu
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-11-28
Journal Detail:
Title:  Cell biochemistry and function     Volume:  -     ISSN:  1099-0844     ISO Abbreviation:  Cell Biochem. Funct.     Publication Date:  2014 Nov 
Date Detail:
Created Date:  2014-11-28     Completed Date:  -     Revised Date:  2014-11-29    
Medline Journal Info:
Nlm Unique ID:  8305874     Medline TA:  Cell Biochem Funct     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014 John Wiley & Sons, Ltd.
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