Document Detail

Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress.
MedLine Citation:
PMID:  18323739     Owner:  NLM     Status:  MEDLINE    
Ischemic postconditioning (I-postC) is a newly discovered endogenous protective phenomenon capable of protecting the myocardium from I/R injury. The cardioprotective mechanisms of I-postC involve protein synthesis and preventing an increase in cytosolic calcium. Endoplasmic reticulum (ER) is a principal site for secretory protein synthesis and calcium storage. Myocardial I/R causes ER stress and perturbations of ER function. The purpose of the present study was to determine whether I-postC's attenuation of I/R injury involves reductions in ER stress through mitogen-activated protein kinase (MAPK) pathway. In the present study, models of rat myocardial I/R and hypoxia/reoxygenation (H/R) of neonatal rat cardiomyocytes were used. Myocardial infarct size was measured by triphenyltetrazolium chloride staining, and flow cytometry was used to quantitate cardiomyocyte apoptosis. Calreticulin expression and activation of caspase 12, p38 MAPK, and c-Jun NH2-terminal kinase (JNK) in myocardium or cardiomyocytes were detected by Western blots. It is found that I-postC protects the I/R heart against myocardial infarction, and hypoxic postconditioning protects neonatal cardiomyocytes from H/R-induced apoptosis. Ischemic postconditioning suppressed I/R-induced ER stress, as shown by a decrease in calreticulin expression and caspase 12 activation. Hypoxic postconditioning up-regulates p38 MAPK phosphorylation and down-regulates JNK phosphorylation in cardiomyocytes subjected to H/R. These results indicate that I-postC protects myocardium from I/R injury by suppressing ER stress, and that p38 MAPK and JNK pathways are associated with the I-postC-induced suppression of ER stress.
Xiu-Hua Liu; Zhen-Ying Zhang; Sheng Sun; Xu-Dong Wu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  30     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-19     Completed Date:  2008-11-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  422-7     Citation Subset:  IM    
Department of Pathophysiology, PLA General Hospital, Beijing, China.
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MeSH Terms
Caspase 12 / metabolism
Cells, Cultured
Endoplasmic Reticulum / metabolism*
Enzyme Activation
Heart / physiology
Ischemic Preconditioning, Myocardial*
MAP Kinase Kinase 4 / metabolism
Myocardium / metabolism*
Myocytes, Cardiac / metabolism
Rats, Wistar
Reperfusion Injury / metabolism*
Signal Transduction
Reg. No./Substance:
EC Kinase Kinase 4; EC 3.4.22.-/Caspase 12

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