Mitochondrial dysfunction reduces the activity of KIR2.1 K⁺ channel in myoblasts via impaired oxidative phosphorylation.
10.4196/kjpp.2018.22.6.697
- Author:
JooHan WOO
1
;
Hyun Jong KIM
;
Yu Ran NAM
;
Yung Kyu KIM
;
Eun Ju LEE
;
Inho CHOI
;
Sung Joon KIM
;
Wan LEE
;
Joo Hyun NAM
Author Information
1. Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea.
- Publication Type:Original Article
- Keywords:
Inward-rectifying K⁺ channel;
MtDNA-depleted myoblasts;
Myoblast;
Myogenesis;
Oxidative phosphorylation
- MeSH:
Antimycin A;
Down-Regulation;
Electron Transport;
Ion Channels;
Membrane Potentials;
Mitochondria;
Muscle Development;
Muscle Fibers, Skeletal;
Myoblasts*;
Oxidative Phosphorylation*
- From:The Korean Journal of Physiology and Pharmacology
2018;22(6):697-703
- CountryRepublic of Korea
- Language:English
-
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 (I(Kir)) 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 I(Kir). The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca²⁺]ᵢ. Our results demonstrated the specific downregulation of I(Kir) by dysfunctional mitochondria. The resultant depolarization and altered Ca²⁺ signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.
