Journal
BIOLOGICAL & PHARMACEUTICAL BULLETIN
Volume 40, Issue 9, Pages 1551-1555Publisher
PHARMACEUTICAL SOC JAPAN
DOI: 10.1248/bpb.b17-00079
Keywords
mitochondria; SEA0400; ischemia-reperfusion; Ca2+ imaging
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Funding
- Japan Society for the Promotion of Science (JSPS) KAKENHI [JP20890233, JP15K08247]
- Grants-in-Aid for Scientific Research [17K15460, 15K08247, 15K07871] Funding Source: KAKEN
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We investigated the effect on mitochondrial Ca2+ of SEA0400, an inhibitor of the Na+/Ca2+ exchanger (NCX) which reduces mitochondrial Ca2+ overload during myocardial ischemia, in digitonin-permeabilized H9c2 cells expressing the mitochondrial-targeted Ca2+ indicator, yellow cameleon 3.1. The elevation of mitochondrial Ca2+ concentration caused by an increase in extramitochondrial Ca2+ concentration was inhibited by carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) or ruthenium red, but enhanced by CGP-37157, a mitochondrial NCX inhibitor. SEA0400 had no effect on mitochondrial Ca2+ under normal and ischemic conditions. Thus, the mitochondria-protective effects of SEA0400 could be explained by inhibition of plasmalemmal NCX but not mitochondrial NCX.
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