Hypoxic postconditioning inhibits endoplasmic reticulum stress-mediated cardiomyocyte apoptosis by targeting PUMA.
Postconditioning prevents cardiomyocytes from ischemia/reperfusion-induced apoptosis. However, little is known about the molecular mechanisms that mediate the cardioprotective effect of postconditioning. Here, we hypothesized that postconditioning targeted p53 upregulated modulator of apoptosis (PUMA) to protect cardiomyocytes against endoplasmic reticulum stress-mediated apoptosis. Our results demonstrated that postconditioning could inhibit GRP78 (78-kDa glucose-regulated protein) expression, caspase-12 activation, and cardiomyocyte apoptosis by regulating PUMA expression. In addition, p53 is involved in the regulatory role of postconditioning in PUMA expression. Our data reveal a cardioprotective pathway of postconditioning in which it represses PUMA.
Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, China. yuzlif96@yahoo.com.cn
YuZhen
Y
Li
ZhenRong
Z
Lv
XiuHua
X
Liu
WenTing
W
Su
Chen
C
Wang
Nana
N
Li
Dandan
D
Song
Tianqi
T
Tao
D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000502:physiology*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D015687:Cell Hypoxia / Q000502:physiology; D002478:Cells, Cultured; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D057775:Ischemic Postconditioning / Q000379:methods*; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D051017:Apoptosis Regulatory Proteins; C533952:Bbc3 protein, rat