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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.

Author information

1
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
2
Department of Physiology, Dongguk University College of Medicine, Gyeongju 38066, Korea.
3
Channelopathy Research Center (CRC), Dongguk University College of Medicine, Goyang 10326, Korea.
4
Department of Medical Biotechnology, Yeungnam University, Gyeongsan 38541, Korea.
5
Department of Biochemistry, Dongguk University College of Medicine, Gyeongju 38066, Korea.

Abstract

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.

KEYWORDS:

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

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