title: Apolipoprotein-J prevention of fetal cardiac myoblast apoptosis induced by ethanol.
abstract: 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.
authors.affiliation: Texas Heart Institute and The University of Texas Health Science Center, Houston, TX 77030, USA.
authors.forename: Yangxin
authors.initials: Y
authors.lastname: Li
authors.forename: Madi Bidya
authors.initials: MB
authors.lastname: Sagar
authors.forename: Michael
authors.initials: M
authors.lastname: Wassler
authors.forename: Harnath
authors.initials: H
authors.lastname: Shelat
authors.forename: Yong-Jian
authors.initials: YJ
authors.lastname: Geng
mesh_terms: 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*
chemical_list: D002316:Cardiotonic Agents; D051152:Clusterin; D000431:Ethanol