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KMID : 0811720180220060697
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Korean Journal of Physiology & Pharmacology
2018 Volume.22 No. 6 p.697 ~ p.703
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Mitochondrial dysfunction reduces the activity of KIR2.1 K+ channel in myoblasts via impaired oxidative phosphorylation
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Woo Joo-Han
Kim Hyun-Jong
Nam Yu-Ran
Kim Yung-Kyu
Lee Eun-Ju
Choi In-Ho
Kim Sung-Joon
Lee Wan
Nam Joo-Hyun
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Abstract
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Myoblast fusion depends on mitochondrial integrity and intracellular Ca2+ signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with [Ca2+]i regulation in normal and mitochondrial DNA-depleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube formation. The inwardly rectifying K+ current (IKir) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated Ca2+ channel and Ca2+-activated K+ channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the IKir. The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca2+]i. Our results demonstrated the specific downregulation of IKir by dysfunctional mitochondria. The resultant depolarization and altered Ca2+ signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.
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KEYWORD
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Inward-rectifying K+ channel, MtDNA-depleted myoblasts, Myoblast, Myogenesis, Oxidative phosphorylation
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