Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10769259 | Biochemical and Biophysical Research Communications | 2005 | 8 Pages |
Abstract
Carbon monoxide (CO) is known to protect myocardial and vascular cells against injuries due to ischemia-reperfusion or inflammation. We showed that a Ca2+-dependent protease calpain promotes necrotic cell death of cardiomyocyte-derived H9c2 cells due to hypoxia through α-fodrin proteolysis. Here, we show that ischemia induces necrotic cell death, which is inhibited by either CO, extracellular Ca2+ deprivation or L-type Ca2+ channel blockers. A whole cell patch-clamp experiment supports that CO inhibits L-type Ca2+ channel mediated influx of Ca2+ and the ischemic death of H9c2 cells.
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Authors
Koichi Uemura, Satomi Adachi-Akahane, Kaori Shintani-Ishida, Ken-ichi Yoshida,