Document Detail

Effects of exercise training on cardiac function and myocardial remodeling in post myocardial infarction rats.
MedLine Citation:
PMID:  17980387     Owner:  NLM     Status:  MEDLINE    
To test the hypothesis that early exercise training after myocardial infarction (MI) could preserve cardiac function, alleviate left ventricular (LV) remodeling and induce a protective effect on morphology, male Sprague-Dawley rats underwent coronary ligation or sham operation, and were assigned to 3 groups: Sham, sedentary MI (SedMI), and exercise MI (ExMI). We measured the changes in collagen volume fraction, matrix metalloproteinase (MMP) 1, tissue inhibitor matrix metalloproteinase 1 (TIMP-1), angiotensin II receptor type 1 (AT1), and angiotensin converting enzyme (ACE) at gene and protein levels after 8 weeks of exercise training. Cardiac functions were determined by echocardiographic and hemodynamic measurements. Early exercise training after MI had no effect on LV wall thinning. Cardiac function was significantly preserved in the ExMI group in comparison to the SedMI group. The collagen volume fraction in the ExMI group was significantly lower than in the SedMI group. Compared to the SedMI group, the ExMI group showed a markedly decrease at both the gene and protein levels in TIMP-1 (P<0.05). No significant differences were found in MMP-1 among the three groups. MMP-1/TIMP-1 ratio in the ExMI group was significantly higher than in the SedMI group. In addition, the expression of AT1 protein in the ExMI group was significantly lower than in the SedMI group. Furthermore, both ACE mRNA expression and ACE binding in the ExMI group are significantly decreased compared to the SedMI group. Our results suggest that early exercise training after MI reduces TIMP-1 expression, improves the balance between MMPs and TIMPs, and mitigates the expressions of ACE and AT1 receptor. These improvements, in turn, attenuate myocardial fibrosis and preserve post-MI cardiac function.
Xiaohua Xu; Wenhan Wan; Anthony S Powers; Ji Li; Lisa L Ji; Shunhua Lao; Bryan Wilson; John M Erikson; John Q Zhang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2007-10-12
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  44     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-31     Completed Date:  2008-03-06     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  114-22     Citation Subset:  IM    
Laboratory of Cardiovascular Research, University of Texas at San Antonio, 1 UTSA Circle, San Antonio, TX 78249, USA.
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MeSH Terms
Blotting, Western
Collagen / metabolism
Collagen Type I / genetics,  metabolism
Collagen Type III / genetics,  metabolism
Fibroblasts / metabolism,  pathology
Gene Expression Regulation
Heart Ventricles / enzymology,  pathology,  physiopathology
Macrophages / pathology
Matrix Metalloproteinase 1 / genetics,  metabolism
Myocardial Infarction / enzymology,  pathology,  physiopathology*,  ultrasonography
Peptidyl-Dipeptidase A / genetics,  metabolism
Physical Conditioning, Animal*
Protein Binding
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 / genetics,  metabolism
Tissue Inhibitor of Metalloproteinase-1 / genetics,  metabolism
Transforming Growth Factor beta1 / genetics,  metabolism
Ventricular Function, Left / physiology*
Ventricular Remodeling / physiology*
Grant Support
R01 HL074273-01A1/HL/NHLBI NIH HHS; R01 HL074273-02/HL/NHLBI NIH HHS; R01 HL074273-03/HL/NHLBI NIH HHS; R01-HL074273/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Collagen Type I; 0/Collagen Type III; 0/Receptor, Angiotensin, Type 1; 0/Tissue Inhibitor of Metalloproteinase-1; 0/Transforming Growth Factor beta1; 9007-34-5/Collagen; EC A; EC Metalloproteinase 1

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