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

Myoblast fusion depends on mitochondrial integrity and intracellular Ca signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with [Ca ] regulation in normal and mitochondrial DNA-depleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube...

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Published in:The Korean journal of physiology & pharmacology 2018, 22(6), , pp.697-703
Main Authors: Woo, JooHan, Kim, Hyun Jong, Nam, Yu Ran, Kim, Yung Kyu, Lee, Eun Ju, Choi, Inho, Kim, Sung Joon, Lee, Wan, Nam, Joo Hyun
Format: Article
Language:English
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약리학
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Summary:Myoblast fusion depends on mitochondrial integrity and intracellular Ca signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with [Ca ] regulation in normal and mitochondrial DNA-depleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube formation. The inwardly rectifying K current (I ) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated Ca channel and Ca -activated K channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the I . The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca ] . Our results demonstrated the specific downregulation of I by dysfunctional mitochondria. The resultant depolarization and altered Ca signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.
ISSN:1226-4512
2093-3827
DOI:10.4196/kjpp.2018.22.6.697