Document Detail


Cardioselective overexpression of HO-1 prevents I/R-induced cardiac dysfunction and apoptosis.
MedLine Citation:
PMID:  12124217     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Heme oxygenase (HO)-1 converts heme to bilirubin, carbon monoxide, and iron. Our prior work has suggested a cardioprotective role for HO-1 in heart failure. To test whether HO-1 (heat shock protein 32) prevents cardiomyocyte apoptosis and cardiac dysfunction after ischemia-reperfusion (I/R), we generated transgenic mice overexpressing HO-1 in the heart under the control of the alpha-myosin heavy chain promoter. HO-1 transcript and protein increased markedly in the heart only. In an isolated heart preparation, we observed an enhanced functional recovery during reperfusion after ischemia in the transgenic hearts compared with nontransgenic controls. I/R injury was also performed in intact animals by coronary ligation and reperfusion to assess the protective role of HO-1 overexpression on heart apoptosis. HO-1 overexpression reduced cardiac apoptosis, as evidenced by fewer terminal deoxynucleodidyl transferase-mediated dUTP nick-end labeling-positive or in situ oligo ligation-positive myocytes, compared with nontransgenic mice. Our results indicate that cardioselective overexpression of HO-1 exerts a cardioprotective effect after myocardial I/R in mice, and this effect is probably mediated via an antiapoptotic action of HO-1.
Authors:
Sreesatya Raju Vulapalli; Zhongyi Chen; Balvin H L Chua; Tingchung Wang; Chang-Seng Liang
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  283     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-07-18     Completed Date:  2002-08-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H688-94     Citation Subset:  IM    
Affiliation:
Cardiology Unit, Department of Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue, Rochester, NY 14642, USA. raju_vulapalli@urmc.rochester.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects*
Coronary Disease / physiopathology
Heart / drug effects,  physiopathology
Heme Oxygenase (Decyclizing) / genetics,  metabolism*
Heme Oxygenase-1
Humans
Membrane Proteins
Mice
Mice, Inbred C57BL
Mice, Transgenic / genetics
Myocardial Ischemia / physiopathology*
Myocardial Reperfusion Injury / physiopathology*
Myocardium / enzymology*
Perfusion
Ventricular Dysfunction, Left / prevention & control*
Grant Support
ID/Acronym/Agency:
HL 68151/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Proteins; EC 1.14.99.3/HMOX1 protein, human; EC 1.14.99.3/Heme Oxygenase (Decyclizing); EC 1.14.99.3/Heme Oxygenase-1; EC 1.14.99.3/Hmox1 protein, mouse

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