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1 Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences,Nagoya City University, Nagoya, Aichi, Japan
* To whom correspondence should be addressed. E-mail: yimaizum{at}phar.nagoya-cu.ac.jp.
The molecular components of large-conductance Ca2+-activated K+ channels, which are functionally expressed in mitochondria (mitoKCa) in cardiac myocytes, have not been identified. Our experimental results show that the transcript corresponding to the large-conductance Ca2+-activated K+ channel 
1 subunit (BK1) is substantially expressed in mammalian heart. A yeast two-hybrid assay showed the BK1 protein can interact with a mitochondrial protein, cytochrome c oxidase subunit I (Cco1). Results from immunocytochemical experiments also demonstrated that BK1 interacted with Cco1 and co-localized in rat cardiac mitochondria. Furthermore, 17-estradiol, which enhances the activity of the BK channel 
subunit only in the presence of the 1 subunit, significantly increased flavoprotein oxidation in rat ventricle myocytes and decreased the rate of cell death under simulated ischemia. Single channel recordings from mitochondrial inner membrane indicated that the activity of mitoKCa, which had a conductance of approximately 270 pS, was enhanced by 17-estradiol and blocked by paxilline. In combination, the present study revealed a new mechanism for the cardioprotective effects of 17-estradiol, which include the activation of mitoKCa via the interaction with BK1. BK1 may be an important molecular component, which functionally couples with both Cco1 and mitoKCa pore-forming subunit.
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