Disparate regulation of signaling proteins after exercise and myocardial infarction.
BACKGROUND
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.


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.
Gosselin
Hugues
H
Research Centre, Montreal Heart Institute, Montreal, Quebec, Canada.
Béliveau
Louise
L
Burelle
Yan
Y
Clément
Robert
R
Lajoie
Claude
C
El-Helou
Viviane
V
Calderone
Angelino
A
D000818:Animals; D003324:Coronary Artery Disease; D005260:Female; D009203:Myocardial Infarction / Q000201:enzymology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt / Q000097:blood; D011792:Quebec; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology*
D051057:Proto-Oncogene Proteins c-akt