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Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan
Submitted 7 January 2005 ; accepted in final form 27 May 2005
The molecular components of the large-conductance Ca2+-activated K+ channels that 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 (BK-1) is substantially expressed in mammalian heart. A yeast two-hybrid assay showed the BK-1 protein can interact with a mitochondrial protein, cytochrome c oxidase subunit I (Cco1). Results from immunocytochemical experiments also demonstrated that BK-1 interacted with Cco1 and colocalized 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 
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 BK-1. BK-1 may be an important molecular component that functionally couples with both Cco1 and mitoKCa pore-forming -subunit.
BK channel 1-subunit; 1-subunit; cytochrome c oxidase; cardioprotection
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