Wojtovich Andrew P, Burwell Lindsay S, Sherman Teresa A, Nehrke Keith W, Brookes Paul S
Department of Pharmacology & Physiology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
Biochem Biophys Res Commun. 2008 Nov 21;376(3):625-8. doi: 10.1016/j.bbrc.2008.09.043. Epub 2008 Sep 20.
Ischemic preconditioning (IPC) is an evolutionarily conserved endogenous mechanism whereby short periods of non-lethal exposure to hypoxia alleviate damage caused by subsequent ischemia reperfusion (IR). Pharmacologic targeting has suggested that the mitochondrial ATP-sensitive potassium channel (mK(ATP)) is central to IPC signaling, despite its lack of molecular identity. Here, we report that isolated Caenorhabditis elegans mitochondria have a K(ATP) channel with the same physiologic and pharmacologic characteristics as the vertebrate channel. Since C. elegans also exhibit IPC, our observations provide a framework to study the role of mK(ATP) in IR injury in a genetic model organism.
缺血预处理(IPC)是一种进化上保守的内源性机制,通过短时间非致死性低氧暴露减轻随后的缺血再灌注(IR)所造成的损伤。药物靶向研究表明,线粒体ATP敏感性钾通道(mK(ATP))是IPC信号传导的核心,尽管其分子身份尚不明确。在此,我们报告分离出的秀丽隐杆线虫线粒体具有一个K(ATP)通道,其生理和药理特性与脊椎动物的通道相同。由于秀丽隐杆线虫也表现出IPC,我们的观察结果为在遗传模式生物中研究mK(ATP)在IR损伤中的作用提供了一个框架。