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
en En
| WPRIM
| ID: wpr-727855
Biblioteca responsable:
WPRO
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.
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Índice:
WPRIM
Asunto principal:
Fosforilación Oxidativa
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Regulación hacia Abajo
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Fibras Musculares Esqueléticas
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Desarrollo de Músculos
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Mioblastos
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Transporte de Electrón
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Canales Iónicos
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Potenciales de la Membrana
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Mitocondrias
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Antimicina A
Idioma:
En
Revista:
The Korean Journal of Physiology and Pharmacology
Año:
2018
Tipo del documento:
Article