Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor

Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one appr...
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Autor*in:	Jin Young Lee [verfasserIn] Da Ae Kim [verfasserIn] Eunah Choi [verfasserIn] Yun Sun Lee [verfasserIn] So Jeong Park [verfasserIn] Beom-Jun Kim [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch ; Koreanisch

Erschienen:	2021

Schlagwörter:	aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress

Übergeordnetes Werk:	In: Endocrinology and Metabolism - Korean Endocrine Society, 2016, 36(2021), 4, Seite 865-874
Übergeordnetes Werk:	volume:36 ; year:2021 ; number:4 ; pages:865-874

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3803/EnM.2021.1108

Katalog-ID:	DOAJ063097540

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520			\|a Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients.
650		4	\|a aldosterone
650		4	\|a sarcopenia
650		4	\|a muscle development
650		4	\|a receptors
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650		4	\|a oxidative stress
653		0	\|a Diseases of the endocrine glands. Clinical endocrinology
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allfields	10.3803/EnM.2021.1108 doi (DE-627)DOAJ063097540 (DE-599)DOAJ1991797a0c234d3da71f4b8ad20915bc DE-627 ger DE-627 rakwb eng kor RC648-665 Jin Young Lee verfasserin aut Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients. aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress Diseases of the endocrine glands. Clinical endocrinology Da Ae Kim verfasserin aut Eunah Choi verfasserin aut Yun Sun Lee verfasserin aut So Jeong Park verfasserin aut Beom-Jun Kim verfasserin aut In Endocrinology and Metabolism Korean Endocrine Society, 2016 36(2021), 4, Seite 865-874 (DE-627)810542803 (DE-600)2802452-7 20935978 nnns volume:36 year:2021 number:4 pages:865-874 https://doi.org/10.3803/EnM.2021.1108 kostenfrei https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc kostenfrei http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf kostenfrei https://doaj.org/toc/2093-596X Journal toc kostenfrei https://doaj.org/toc/2093-5978 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 36 2021 4 865-874
spelling	10.3803/EnM.2021.1108 doi (DE-627)DOAJ063097540 (DE-599)DOAJ1991797a0c234d3da71f4b8ad20915bc DE-627 ger DE-627 rakwb eng kor RC648-665 Jin Young Lee verfasserin aut Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients. aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress Diseases of the endocrine glands. Clinical endocrinology Da Ae Kim verfasserin aut Eunah Choi verfasserin aut Yun Sun Lee verfasserin aut So Jeong Park verfasserin aut Beom-Jun Kim verfasserin aut In Endocrinology and Metabolism Korean Endocrine Society, 2016 36(2021), 4, Seite 865-874 (DE-627)810542803 (DE-600)2802452-7 20935978 nnns volume:36 year:2021 number:4 pages:865-874 https://doi.org/10.3803/EnM.2021.1108 kostenfrei https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc kostenfrei http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf kostenfrei https://doaj.org/toc/2093-596X Journal toc kostenfrei https://doaj.org/toc/2093-5978 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 36 2021 4 865-874
allfields_unstemmed	10.3803/EnM.2021.1108 doi (DE-627)DOAJ063097540 (DE-599)DOAJ1991797a0c234d3da71f4b8ad20915bc DE-627 ger DE-627 rakwb eng kor RC648-665 Jin Young Lee verfasserin aut Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients. aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress Diseases of the endocrine glands. Clinical endocrinology Da Ae Kim verfasserin aut Eunah Choi verfasserin aut Yun Sun Lee verfasserin aut So Jeong Park verfasserin aut Beom-Jun Kim verfasserin aut In Endocrinology and Metabolism Korean Endocrine Society, 2016 36(2021), 4, Seite 865-874 (DE-627)810542803 (DE-600)2802452-7 20935978 nnns volume:36 year:2021 number:4 pages:865-874 https://doi.org/10.3803/EnM.2021.1108 kostenfrei https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc kostenfrei http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf kostenfrei https://doaj.org/toc/2093-596X Journal toc kostenfrei https://doaj.org/toc/2093-5978 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 36 2021 4 865-874
allfieldsGer	10.3803/EnM.2021.1108 doi (DE-627)DOAJ063097540 (DE-599)DOAJ1991797a0c234d3da71f4b8ad20915bc DE-627 ger DE-627 rakwb eng kor RC648-665 Jin Young Lee verfasserin aut Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients. aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress Diseases of the endocrine glands. Clinical endocrinology Da Ae Kim verfasserin aut Eunah Choi verfasserin aut Yun Sun Lee verfasserin aut So Jeong Park verfasserin aut Beom-Jun Kim verfasserin aut In Endocrinology and Metabolism Korean Endocrine Society, 2016 36(2021), 4, Seite 865-874 (DE-627)810542803 (DE-600)2802452-7 20935978 nnns volume:36 year:2021 number:4 pages:865-874 https://doi.org/10.3803/EnM.2021.1108 kostenfrei https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc kostenfrei http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf kostenfrei https://doaj.org/toc/2093-596X Journal toc kostenfrei https://doaj.org/toc/2093-5978 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 36 2021 4 865-874
allfieldsSound	10.3803/EnM.2021.1108 doi (DE-627)DOAJ063097540 (DE-599)DOAJ1991797a0c234d3da71f4b8ad20915bc DE-627 ger DE-627 rakwb eng kor RC648-665 Jin Young Lee verfasserin aut Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients. aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress Diseases of the endocrine glands. Clinical endocrinology Da Ae Kim verfasserin aut Eunah Choi verfasserin aut Yun Sun Lee verfasserin aut So Jeong Park verfasserin aut Beom-Jun Kim verfasserin aut In Endocrinology and Metabolism Korean Endocrine Society, 2016 36(2021), 4, Seite 865-874 (DE-627)810542803 (DE-600)2802452-7 20935978 nnns volume:36 year:2021 number:4 pages:865-874 https://doi.org/10.3803/EnM.2021.1108 kostenfrei https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc kostenfrei http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf kostenfrei https://doaj.org/toc/2093-596X Journal toc kostenfrei https://doaj.org/toc/2093-5978 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 36 2021 4 865-874
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author	Jin Young Lee
spellingShingle	Jin Young Lee misc RC648-665 misc aldosterone misc sarcopenia misc muscle development misc receptors misc mineralocorticoid misc oxidative stress misc Diseases of the endocrine glands. Clinical endocrinology Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor
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topic_title	RC648-665 Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor aldosterone sarcopenia muscle development receptors mineralocorticoid oxidative stress
topic	misc RC648-665 misc aldosterone misc sarcopenia misc muscle development misc receptors misc mineralocorticoid misc oxidative stress misc Diseases of the endocrine glands. Clinical endocrinology
topic_unstemmed	misc RC648-665 misc aldosterone misc sarcopenia misc muscle development misc receptors misc mineralocorticoid misc oxidative stress misc Diseases of the endocrine glands. Clinical endocrinology
topic_browse	misc RC648-665 misc aldosterone misc sarcopenia misc muscle development misc receptors misc mineralocorticoid misc oxidative stress misc Diseases of the endocrine glands. Clinical endocrinology
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title	Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor
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title_sort	aldosterone inhibits in vitro myogenesis by increasing intracellular oxidative stress via mineralocorticoid receptor
callnumber	RC648-665
title_auth	Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor
abstract	Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients.
abstractGer	Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients.
abstract_unstemmed	Background Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reverse-transcription 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-dependent manner, 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 due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular 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 sarcopenia in these patients.
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title_short	Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor
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A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone. 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Metabolism</subfield><subfield code="d">Korean Endocrine Society, 2016</subfield><subfield code="g">36(2021), 4, Seite 865-874</subfield><subfield code="w">(DE-627)810542803</subfield><subfield code="w">(DE-600)2802452-7</subfield><subfield code="x">20935978</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:36</subfield><subfield code="g">year:2021</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:865-874</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.3803/EnM.2021.1108</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/1991797a0c234d3da71f4b8ad20915bc</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://www.e-enm.org/upload/pdf/enm-2021-1108.pdf</subfield><subfield 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Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor

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