Document Detail

Attenuating ischemia-induced H9c2 myoblasts apoptosis by therapeutic hypothermia.
MedLine Citation:
PMID:  20220335     Owner:  NLM     Status:  MEDLINE    
Although inducing mild hypothermia (32 degrees C) in animal models of cardiac arrest with highly attenuated cardiac and neurological injury, the protective effects of hypothermia molecular mechanisms were not fully elucidated, and thus, were examined here on the H9c2 rat ventricular myoblasts that underwent cell loss as well as apoptosis in conditions of simulated ischemia, represented by serum withdrawal plus hypoxia. The H9c2 cells apoptosis was evidenced by flow cytometry-, DNA fragmentation-, and caspase 3 activation-increased apoptotic cells (Annexin-V positive and propidium iodide negative). For the simulated ischemia, both cell loss and apoptosis of these cardiomyoblasts were associated with downregulated small molecular weight proteins (heat shock protein 20, heat shock protein 27, and alphaB-crystallin). Mild hypothermia significantly reduced the ischemia-induced apoptosis, small molecular weight proteins downregulation, and cell viability cut. Conclusively, hypothermia may inhibit simulated ischemia-induced apoptosis in cardiomyocytes by restoring normal small molecular weight proteins expression.
Cheng-Hsin Lin; Wen-Shiann Wu; Mao-Tsun Lin; Wen-Ping Liu; Ron-Bin Hsu; Ching-Ping Chang
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of the medical sciences     Volume:  339     ISSN:  1538-2990     ISO Abbreviation:  Am. J. Med. Sci.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-11     Completed Date:  2010-04-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370506     Medline TA:  Am J Med Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  258-65     Citation Subset:  AIM; IM    
Graduate Institute of Clinical Medicine and Department of Surgery, National Taiwan University School of Medicine, Taipei, Taiwan.
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MeSH Terms
Apoptosis / physiology*
Cell Hypoxia / physiology
Cell Line
Cell Survival / physiology
DNA Fragmentation
Hypothermia, Induced* / adverse effects
Myoblasts / metabolism*,  pathology

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