Document Detail


p38 mitogen-activated protein kinase inhibition improves cardiac function and attenuates left ventricular remodeling following myocardial infarction in the rat.
MedLine Citation:
PMID:  15489104     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The aim of this study was to examine the effect of the p38 mitogen-activated protein kinase (MAPK) inhibitor, RWJ-67657 (RWJ), on left ventricular (LV) dysfunction and remodeling post-myocardial infarction (MI) in rats. BACKGROUND: p38 MAPK signaling has been implicated in the progression of chronic heart failure. METHODS: From day 7 post-MI (coronary artery ligation), rats received either RWJ (50 mg/day, by gavage, n = 8, MI+RWJ) or vehicle (by gavage, n = 8, MI+V) for 21 days. Echocardiography was performed on day 6, before the commencement of treatment, and on day 27. In vivo hemodynamic measurements were made on day 28. Sham-operated rats served as controls. RESULTS: The LV end-diastolic pressure and lung/body weight ratio were reduced, whereas the maximum rate of rise of LV pressure was increased towards sham levels in MI+RWJ compared with MI+V. Baseline echocardiographic studies demonstrated uniform LV remodeling and dysfunction in MI rats. Fractional shortening (FS) further deteriorated in MI+V, whereas FS was preserved in MI+RWJ. Progressive LV dilation and infarct expansion observed in MI+V were inhibited in MI+RWJ. MI+RWJ also demonstrated increased myocyte hypertrophy in the peri-infarct and non-infarct zones, and reduced myocardial collagen and alpha-smooth muscle actin (SMA) immunoreactivity compared with MI+V. The antifibrotic effects of RWJ in vivo may reflect direct effects on cardiac fibroblasts, because RWJ attenuated transforming growth factor beta-1-stimulated collagen synthesis and alpha-SMA expression in isolated cardiac fibroblasts. RWJ also protected cultured myocytes from hydrogen peroxide-induced apoptosis. CONCLUSIONS: RWJ-67657 treatment post-MI had beneficial effects on LV remodeling and dysfunction, supporting a key role for p38 MAPK in pathologic cell signaling in these processes and its inhibition as a novel therapy.
Authors:
Fiona See; Walter Thomas; Kerrie Way; Alex Tzanidis; Andrew Kompa; Dion Lewis; Silviu Itescu; Henry Krum
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  44     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-10-18     Completed Date:  2004-11-30     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1679-89     Citation Subset:  AIM; IM    
Affiliation:
National Health and Medical Research Council Center of Clinical Research Excellence in Therapeutics, Department of Medicine, Monash University, Alfred Hospital, Commercial Road, Prahran, Victoria 3181, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects,  physiology
Cells, Cultured
Collagen Type I / metabolism
Collagen Type II / metabolism
Echocardiography
Enzyme Inhibitors / pharmacology*
Female
Hemodynamics / drug effects,  physiology
Imidazoles / pharmacology*
Immunoenzyme Techniques
Myocardial Contraction / drug effects,  physiology
Myocardial Infarction / pathology,  physiopathology*
Myocardium / pathology
Myocytes, Cardiac / drug effects,  pathology,  physiology
Pyridines / pharmacology*
Rats
Rats, Sprague-Dawley
Signal Transduction / drug effects,  physiology
Ventricular Dysfunction, Left / pathology,  physiopathology
Ventricular Remodeling / drug effects*,  physiology
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors*,  physiology
Chemical
Reg. No./Substance:
0/Collagen Type I; 0/Collagen Type II; 0/Enzyme Inhibitors; 0/Imidazoles; 0/Pyridines; 0/RWJ 67657; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases

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