Mitochondrial dysfunction reduces the activity of KIR2.1 K⁺ channel in myoblasts via impaired oxidative phosphorylation
The Korean Journal of Physiology and Pharmacology
;
: 697-703, 2018.
Article
in English
| WPRIM
| ID: wpr-727855
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Oxidative Phosphorylation
/
Down-Regulation
/
Muscle Fibers, Skeletal
/
Muscle Development
/
Myoblasts
/
Electron Transport
/
Ion Channels
/
Membrane Potentials
/
Mitochondria
/
Antimycin A
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2018
Type:
Article
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