Document Detail


Calcineurin is involved in cardioprotection induced by ischemic postconditioning through attenuating endoplasmic reticulum stress.
MedLine Citation:
PMID:  22088531     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
BACKGROUND: Ischemic postconditioning (I-postC) is a newly discovered and more amenable cardioprotective strategy capable of protecting the myocardium from ischemia/reperfusion (I/R) injury. Endoplasmic reticulum (ER) is a principal site for secretary protein synthesis and calcium storage. Myocardial I/R causes ER stress and emerging studies suggest that the cardioprotection has been linked to the modulation of ER stress. The aim of the present study was to determine whether cardioprotection of I-postC involves reduction in ER stress through calcineurin pathway.
METHODS: In the in vivo model of rat myocardial I/R, myocardial infarct size was measured by triphenyltetrazolium chloride (TTC) staining and apoptosis was detected using terminal eoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Expression of calreticulin, C/EBP homologous protein (CHOP), caspase-12, and activation of caspase-12 in myocardium were detected by Western blotting. The activity and expression of calcineurin in myocardium were also detected.
RESULTS: I-postC protected the I/R heart against apoptosis, myocardial infarction, and leakage of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB). I-postC suppressed I/R-induced ER stress, as shown by a decrease in the expression of calreticulin and CHOP, and caspase-12 activation. I-postC downregulated calcineurin activation in myocardium subjected to I/R.
CONCLUSION: I-postC protects myocardium from I/R injury by suppressing ER stress and calcineurin pathways are not associated with the I-postC-induced suppression of ER stress-related apoptosis.
Authors:
Yi-Hong Chen; Xu-Dong Wu; Shu-Tong Yao; Seng Sun; Xiu-Hua Liu
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Chinese medical journal     Volume:  124     ISSN:  0366-6999     ISO Abbreviation:  Chin. Med. J.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-11-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7513795     Medline TA:  Chin Med J (Engl)     Country:  China    
Other Details:
Languages:  eng     Pagination:  3334-40     Citation Subset:  IM    
Affiliation:
Department of Pathophysiology, Chinese People's Liberation Army General Hospital, Beijing 100853, China.
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