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Korean J Physiol Pharmacol. 2018 Nov;22(6):697-703. doi: 10.4196/kjpp.2018.22.6.697. Epub 2018 Oct 25.

Mitochondrial dysfunction reduces the activity of KIR2.1 K+ channel in myoblasts via impaired oxidative phosphorylation.

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Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea.
Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea.
Department of Medical Biotechnology, Yeungnam University, Gyeongsan 38541, Korea.
Department of Biochemistry, Dongguk University College of Medicine, Gyeongju 38066, Korea.


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.


Inward-rectifying K+ channel; MtDNA-depleted myoblasts; Myoblast; Myogenesis; Oxidative phosphorylation

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