Apolipoprotein-J prevention of fetal cardiac myoblast apoptosis induced by ethanol.
Over-consumption of ethanol (EtOH) represents a major health problem. This study was to test the cytotoxicity of EtOH in cardiac stem cells or myoblasts, and the potential protective effect of apolipoprotein-J (ApoJ), a stress-responding, chaperone-like protein in high-density lipoprotein, on EtOH-injured cardiac myoblasts. In culture, EtOH-exposed canine fetal myoblasts underwent apoptosis in a concentration- and time-dependent manner. Expression ApoJ by cDNA transfection markedly reduced EtOH-induced apoptosis in the cells. ApoJ expression also restored partially the mitochondrial membrane potential and prevented the release of cytochrome-c from mitochondria into cytoplasma. Thus, ApoJ serves as a cytoprotective protein that protects cardiac stem cells against EtOH cytotoxicity.
Li
Yangxin
Y
Texas Heart Institute and The University of Texas Health Science Center, Houston, TX 77030, USA.
Sagar
Madi Bidya
MB
Wassler
Michael
M
Shelat
Harnath
H
Geng
Yong-Jian
YJ
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D002316:Cardiotonic Agents / Q000378:metabolism; D002478:Cells, Cultured; D051152:Clusterin / Q000235:genetics / Q000378:metabolism*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage*; D006321:Heart / Q000187:drug effects / Q000196:embryology*; D032386:Myoblasts, Cardiac / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*
D002316:Cardiotonic Agents; D051152:Clusterin; D000431:Ethanol