Uemura Koichi, Adachi-Akahane Satomi, Shintani-Ishida Kaori, Yoshida Ken-ichi
Department of Forensic Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Biochem Biophys Res Commun. 2005 Aug 26;334(2):661-8. doi: 10.1016/j.bbrc.2005.06.142.
Carbon monoxide (CO) is known to protect myocardial and vascular cells against injuries due to ischemia-reperfusion or inflammation. We showed that a Ca(2+)-dependent protease calpain promotes necrotic cell death of cardiomyocyte-derived H9c2 cells due to hypoxia through alpha-fodrin proteolysis. Here, we show that ischemia induces necrotic cell death, which is inhibited by either CO, extracellular Ca(2+) deprivation or L-type Ca(2+) channel blockers. A whole cell patch-clamp experiment supports that CO inhibits L-type Ca(2+) channel mediated influx of Ca(2+) and the ischemic death of H9c2 cells.
众所周知，一氧化碳（CO）可保护心肌和血管细胞免受缺血再灌注或炎症所致的损伤。我们发现，一种钙依赖性蛋白酶钙蛋白酶可通过α-血影蛋白水解作用，促使心肌来源的H9c2细胞因缺氧而发生坏死性细胞死亡。在此，我们表明，缺血可诱导坏死性细胞死亡，而一氧化碳、细胞外钙缺失或L型钙通道阻滞剂均可抑制这种死亡。全细胞膜片钳实验证实，一氧化碳可抑制L型钙通道介导的钙离子内流以及H9c2细胞的缺血性死亡。
