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

• Published in: The Korean journal of physiology & pharmacology Vol. 22; no. 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: Journal Article
• Language: English
• Published: Korea (South) The Korean Physiological Society and The Korean Society of Pharmacology 01.11.2018; 대한약리학회
• Subjects: Original; 약리학; Myoblast; Oxidative phosphorylation; Inward-rectifying K+ channel; MtDNA-depleted myoblasts; Myogenesis
• ISSN: 1226-4512; 2093-3827
• DOI: 10.4196/kjpp.2018.22.6.697

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.