Li Yangxin, Sagar Madi Bidya, Wassler Michael, Shelat Harnath, Geng Yong-Jian
Texas Heart Institute and The University of Texas Health Science Center, Houston, TX 77030, USA.
Biochem Biophys Res Commun. 2007 May 25;357(1):157-61. doi: 10.1016/j.bbrc.2007.03.109. Epub 2007 Mar 28.
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.
乙醇（EtOH）摄入过量是一个主要的健康问题。本研究旨在测试EtOH对心脏干细胞或成肌细胞的细胞毒性，以及载脂蛋白J（ApoJ）（一种存在于高密度脂蛋白中的应激反应性伴侣样蛋白）对EtOH损伤的心脏成肌细胞的潜在保护作用。在培养过程中，暴露于EtOH的犬胎儿成肌细胞以浓度和时间依赖性方式发生凋亡。通过cDNA转染表达ApoJ可显著减少细胞中EtOH诱导的凋亡。ApoJ的表达还部分恢复了线粒体膜电位，并阻止了细胞色素c从线粒体释放到细胞质中。因此，ApoJ作为一种细胞保护蛋白，可保护心脏干细胞免受EtOH的细胞毒性作用。
