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Disparate regulation of signaling proteins after exercise and myocardial infarction.

Authors: Gosselin, H  Beliveau, L  Burelle, Y  Clement, R  Lajoie, C  El-Helou, V  Calderone, A 
Citation: Gosselin H, etal., Med Sci Sports Exerc. 2006 Mar;38(3):455-62.
Pubmed: (View Article at PubMed) PMID:16540832
DOI: Full-text: DOI:10.1249/01.mss.0000205138.02440.79

INTRODUCTION: The signaling proteins extracellular signal-regulated kinase (ERK1/2) and protein kinase B (PKB) were implicated in the development of pathological cardiac hypertrophy. The present study examined whether the progression of physiological eccentric cardiac hypertrophy was associated with ERK1/2 and PKB recruitment. METHODS AND RESULTS: Following 1 and 3 wk of voluntary exercise, female Sprague-Dawley rats ran a total distance of 55 +/- 10 and 195 +/- 19 km, respectively. Left ventricular hypertrophy was detected in 3-wk-exercised rats, albeit prepro-ANP protein expression was unchanged. ERK1/2 was not recruited in the left ventricle (LV) of either 1-wk-exercised rats or the hypertrophied LV of 3-wk-exercised rats. In 1-wk-exercised rats, PKB Thr308 and Ser473 phosphorylation were significantly reduced, whereas a selective increase of PKB Ser473 phosphorylation was observed in the hypertrophied LV of 3-wk-exercised rats. In both 1- and 3-wk-exercised rats, an upward electrophoretic mobility band shift of p70 ribosomal S6 kinase (p70 S6K) was detected. In 1-wk post-myocardial-infarcted (MI) female Sprague-Dawley rats, scar formation was associated with increased left ventricular end-diastolic pressure. In the hypertrophied noninfarcted left ventricle (NILV), ERK1/2, p70 S6K, PKB Ser473, and Thr308 phosphorylation were increased. CONCLUSIONS: These data support the premise that ERK1/2 and PKB were differentially regulated during the development of eccentric physiological and pathological cardiac hypertrophy. It remains to be determined whether the chronic activation of either ERK1/2 and/or PKB in the NILV of post-MI rats may contribute in part to maladaptive cardiac remodelling.

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CRRD Object Information
CRRD ID: 1642998
Created: 2007-11-16
Species: All species
Last Modified: 2007-11-16
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.