학술논문
Mitochondrial dysfunction reduces the activity of KIR2.1 K+ channel in myoblasts via impaired oxidative phosphorylation
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- 영문명
- Mitochondrial dysfunction reduces the activity of KIR2.1 K+ channel in myoblasts via impaired oxidative phosphorylation
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- 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
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제22권 제6호, 697~703쪽, 전체 7쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2018.11.30
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국문 초록
영문 초록
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 DNAdepleted (ρ0) L6 myoblasts. The ρ0 myoblasts showed impaired myotube formation. The inwardly rectifying K+ current (IKir) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated Ca2+ channel and Ca2+-ctivated K+ channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the IKir. The ρ0 myoblasts showed depolarized resting membrane potential and higher basal [Ca2+]i. Our results demonstrated the specific downregulation of IKir by dysfunctional mitochondria. The resultant depolarization and altered Ca2+ signaling might be associated with impaired myoblast fusion in ρ0 myoblasts.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
CONFLICTS OF INTEREST
키워드
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