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A more recent version of this article appeared on March 10, 2006
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M511024200v1
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Papers In Press, published online ahead of print December 30, 2005
J. Biol. Chem, 10.1074/jbc.M511024200
Submitted on October 11, 2005
Revised on December 5, 2005
Accepted on December 30, 2005

Estrogen prevents cardiomyocyte apoptosis through inhibition of reactive oxygen species and differential regulation of p38 kinase isoforms

Jin Kyung Kim, Ali Pedram, Mahnaz Razandi, and Ellis R. Levin

Dept. of Medicine, Long Beach VA Medical Center, Long Beach, CA 90822

Corresponding Author: ellis.levin{at}med.va.gov

From human and animal studies, estrogen is known to protect the myocardium from an ischemic insult. However, there is limited knowledge regarding mechanisms by which estrogen directly protects cardiomyocytes. In this report, we employ an in vitro model, in which cultured rat cardiomyocytes undergo prolonged hypoxia followed by reoxygenation (H/R), in order to study the cardioprotective mechanism of estrogen. 17-ß-estradiol (E2) acting via estrogen receptors (ER) inhibited H/R-induced apoptosis of cardiomyocytes. Mitochondrial reactive oxygen species (ROS) generated from H/R activated p38a MAPK, and inhibition of p38a with SB203580 significantly prevented H/R-induced cell death. E2 suppressed ROS formation and p38a activation by H/R, and concomitantly augmented the activity of p38ß. Unlike p38a, p38ß was little affected by H/R. Dominant negative p38ß protein expression decreased E2-mediated cardiomyocyte survival and ROS suppression during H/R stress. The prosurvival signaling molecule, phosphoinositide-3 kinase (PI3K) has previously been linked to cell survival following ischemia-reperfusion injury. Here, E2-activated PI3K was found to inhibit ROS generated from H/R injury, leading to inhibition of downstream p38a. We further linked these signaling pathways in that p38ß was activated by E2 stimulation of PI3K. Thus, E2 differentially modulates two major isoforms of p38, leading to cardiomyocyte survival. This is achieved by signaling through PI3K, integrating cell survival mediators.


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