Angiotensin II receptor blockade improves matrix metalloproteinases/tissue inhibitor of matrix metalloproteinase-1 balance and restores fibronectin expression in rat infarcted myocardium - PubMed (original) (raw)

. 2009 Oct 23;388(3):606-11.

doi: 10.1016/j.bbrc.2009.08.073. Epub 2009 Aug 18.

Affiliations

• PMID: 19695229
• DOI: 10.1016/j.bbrc.2009.08.073

Angiotensin II receptor blockade improves matrix metalloproteinases/tissue inhibitor of matrix metalloproteinase-1 balance and restores fibronectin expression in rat infarcted myocardium

Dachun Yang et al. Biochem Biophys Res Commun. 2009.

Abstract

Matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs) have been recognized to play a pivotal role in matrix remodeling following myocardial infarction (MI). The aims of the present study were to examine the expression profile of MMPs/TIMP-1 after MI and to determine whether angiotensin II receptor (ATR) blockade improves MMPs/TIMP-1 balance. Compared with sham-operated rats, in vivo MI-induced a significant elevation of MMP-2, MMP-3 and MMP-9 levels and a marked reduction of TIMP-1 and fibronectin (FN) expressions in infarcted left ventricular free wall (LVFW) and hypertrophic interventricular septum (IS) but not in non-infarcted right ventricle (RV). In addition, regional MI increased MMP-2, MMP-3 and MMP-9, while decreased TIMP-1 and FN in infarcted LVFW and hypertrophic IS compared with the non-infarcted RV. Compared with vehicle-treated MI rats, oral valsartan, but not PD123319, limited infarct size, normalized MMPs/TIMP-1 balance and restored FN level. The present findings might further our understanding of the regulatory mechanisms of valsartan in myocardial remodeling after MI.

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