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자료유형
학술저널
저자정보
이진영 (울산대학교) 김다애 (울산대학교) 최은아 (울산대학교) 이윤선 (울산대학교) 박소정 (울산대학교) 김범준 (서울아산병원)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.36 No.4
발행연도
2021.8
수록면
865 - 874 (10page)
DOI
https://doi.org/10.3803/EnM.2021.1108

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Background: Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclearwhether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance orimpaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis andthe potential mechanism explaining it. Methods: Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reversetranscription polymerase chain reaction, Western blot, viability, and migration analyses were performed for experimental research. Results: Recombinant aldosterone treatment suppressed muscle differentiation from mouse C2C12 myoblasts in a dose-dependentmanner, and consistently reduced the expression of myogenic differentiation markers. Furthermore, aldosterone significantly increased intracellular reactive oxygen species (ROS) levels in myotubes, and treatment with N-acetyl cysteine, a potent biological thiol antioxidant, reversed the decrease of myotube area, myotube area per myotube, nucleus number per myotube, and fusion index dueto aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoidreceptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulatedintracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone. Conclusion: These findings support the hypothesis that hypersecretion of aldosterone, like PA, directly contributes to muscular deterioration and suggest that antioxidants and/or MR antagonists could be effective therapeutic options to reduce the risk of sarcopeniain these patients.

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