HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 296/5/H1625    most recent 01057.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Berni, R. Articles by Stilli, D. Search for Related Content PubMed PubMed Citation Articles by Berni, R. Articles by Stilli, D.

Modulation of actin isoform expression before the transition from experimental compensated pressure-overload cardiac hypertrophy to decompensation

¹Department of Evolutionary and Functional Biology, Physiology Section, University of Parma, Italy; and ²Departments of Pathology and Immunology and ³Clinical Pathology, University of Geneva, Switzerland

Submitted 2 October 2008 ; accepted in final form 21 February 2009

In a rat model of long-lasting pressure-overload hypertrophy, we investigated whether changes in the relative expression of myocardial actin isoforms are among the early signs of ventricular mechanical dysfunction before the transition toward decompensation. Forty-four rats with infrarenal aortic banding (AC rats) were studied. Hemodynamic parameters were measured 1 mo (AC₁ group; n = 20) or 2 mo (AC₂; n = 24) after aortic ligature. Then subgroups of AC₁ and AC₂ left ventricles (LV) were used to evaluate 1) LV anatomy and fibrosis (morphometry), 2) expression levels (immunoblotting) and spatial distribution (immunohistochemistry) of alpha-skeletal actin (-SKA), alpha-cardiac actin (-CA), and alpha-smooth muscle actin (-SMA), and 3) cell mechanics and calcium transients in enzimatically isolated myocytes. Although the two AC groups exhibited a comparable degree of hypertrophy (+30% in LV mass; +20% in myocyte surface) and a similar increase in the amount of fibrosis compared with control animals (C group; n = 22), a worsening of LV mechanical performance was observed only in AC₂ rats at both organ and cellular levels. Conversely, AC₁ rats exhibited enhanced LV contractility and preserved cellular contractile behavior associated with increased calcium transients. Alpha-SKA expression was upregulated (+60%) in AC₁. In AC₂ ventricles, prolonged hypertension also induced a significant increase in -SMA expression, mainly at the level of arterial vessels. No significant differences among groups were observed in -CA expression. Our findings suggest that -SKA expression regulation and wall remodeling of coronary arterioles participate in the development of impaired kinetics of contraction and relaxation in prolonged hypertension before the occurrence of marked histopathologic changes.

aortic ligature; hypertension