Document Detail


Exercise-induced HSP-72 elevation and cardioprotection against infarct and apoptosis.
MedLine Citation:
PMID:  17569768     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Successive bouts of endurance exercise are associated with both increased cardiac levels of heat shock protein-72 (HSP-72) and improved cardioprotection against ischemia-reperfusion (I/R)-induced cardiac cell death. Although overexpression of HSP-72 has been shown to be cardioprotective in transgenic animals, it is unclear whether increased levels of HSP-72 are essential for exercise-induced cardioprotection against I/R-mediated cell death. We tested the hypothesis that exercise-induced increases in myocardial levels of HSP-72 are required to achieve exercise-mediated protection against I/R-induced cardiac cell death. To test this postulate, we investigated the effect of preventing the exercise-induced increase in cardiac HSP-72 on myocardial infarction and apoptosis after 50 min of in vivo ischemia and 120 min of reperfusion. Adult male rats remained sedentary or performed successive bouts of endurance exercise in cold (8 degrees C) or warm (22 degrees C) environments. We found that, compared with sedentary control animals, exercise in a warm environment significantly increased myocardial HSP-72 content. In contrast, exercise in the cold environment prevented the exercise-induced increase in myocardial HSP-72 levels. After in vivo myocardial I/R, infarct size was reduced in both exercised groups compared with sedentary animals. Furthermore, compared with sedentary rats, I/R-induced myocardial apoptosis (as indicated by terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling-positive nuclei and caspase-3 activity) was attenuated in both groups of exercised animals. Therefore, although HSP-72 has cardioprotective properties, our results reveal that increased myocardial levels of HSP-72 (above control) are not essential for exercise-induced protection against I/R-induced myocardial infarction and apoptosis.
Authors:
John C Quindry; Karyn L Hamilton; Joel P French; Youngil Lee; Zsolt Murlasits; Nihal Tumer; Scott K Powers
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-06-14
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  103     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-28     Completed Date:  2007-12-20     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1056-62     Citation Subset:  IM    
Affiliation:
Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, Florida, USA. quindryjc@appstate.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
HSP72 Heat-Shock Proteins / metabolism*
Male
Myocardial Infarction / metabolism*
Myocardium / metabolism*
Physical Conditioning, Animal / physiology*
Rats
Rats, Sprague-Dawley
Reperfusion Injury / metabolism*
Grant Support
ID/Acronym/Agency:
F32 HL-74666-02/HL/NHLBI NIH HHS; R01 067855-01//PHS HHS
Chemical
Reg. No./Substance:
0/HSP72 Heat-Shock Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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