
Mitochondrial dysfunction reduces the activity of KIR2.1 K<sup>+</sup> channel in myoblasts via impaired oxidative phosphorylation
Mitochondrial dysfunction reduces the activity of KIR2.1 K<sup>+</sup> channel in myoblasts via impaired oxidative phosphorylation
- Joo Han Woo Hyun Jong Kim Yu Ran Nam Yung Kyu Kim Eun Ju Lee In-ho Choi Sung Joon Kim Wan Lee Joo Hy
- 대한생리학회-대한약리학회
- The Korean Journal of Physiology & Pharmacology
- 제22권 제6호
- 등재여부 : KCI등재
- 2018.11
- 697 - 703 (7 pages)
Myoblast fusion depends on mitochondrial integrity and intracellular Ca<sub>2<sub>+</sub></sub> signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with [Ca<sub>2<sub>+</sub></sub>]<sub>i</sub> regulation in normal and mitochondrial DNAdepleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube formation. The inwardly rectifying K<sub>+</sub> current (I<sub>Kir</sub>) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated Ca<sub>2<sub>+</sub></sub> channel and Ca<sub>2<sub>+</sub></sub>-ctivated K<sub>+</sub> channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the I<sub>Kir</sub>. The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca<sub>2<sub>+</sub></sub>]<sub>i</sub>. Our results demonstrated the specific downregulation of I<sub>Kir</sub> by dysfunctional mitochondria. The resultant depolarization and altered Ca<sub>2<sub>+</sub></sub> signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.
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