Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy

Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle dur...
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Autor*in:	Matthew B. Hudson [verfasserIn] Myra E. Woodworth-Hobbs [verfasserIn] Jennifer L. Gooch [verfasserIn] S. Russ Price [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch ; Koreanisch

Erschienen:	2012

Übergeordnetes Werk:	In: Kidney Research and Clinical Practice - The Korean Society of Nephrology, 2018, 31(2012), 2, p A92
Übergeordnetes Werk:	volume:31 ; year:2012 ; number:2, p A92

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.krcp.2012.04.625

Katalog-ID:	DOAJ04035735X

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520			\|a Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020
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allfieldsGer	10.1016/j.krcp.2012.04.625 doi (DE-627)DOAJ04035735X (DE-599)DOAJa39ad03fb616440780d7c0ac76fe49cd DE-627 ger DE-627 rakwb eng kor RC31-1245 RC581-951 Matthew B. Hudson verfasserin aut Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020 Internal medicine Specialties of internal medicine Myra E. Woodworth-Hobbs verfasserin aut Jennifer L. Gooch verfasserin aut S. Russ Price verfasserin aut In Kidney Research and Clinical Practice The Korean Society of Nephrology, 2018 31(2012), 2, p A92 (DE-627)689392699 (DE-600)2656420-8 22119140 nnns volume:31 year:2012 number:2, p A92 https://doi.org/10.1016/j.krcp.2012.04.625 kostenfrei https://doaj.org/article/a39ad03fb616440780d7c0ac76fe49cd kostenfrei http://www.sciencedirect.com/science/article/pii/S2211913212006584 kostenfrei https://doaj.org/toc/2211-9132 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_2014 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 31 2012 2, p A92
allfieldsSound	10.1016/j.krcp.2012.04.625 doi (DE-627)DOAJ04035735X (DE-599)DOAJa39ad03fb616440780d7c0ac76fe49cd DE-627 ger DE-627 rakwb eng kor RC31-1245 RC581-951 Matthew B. Hudson verfasserin aut Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020 Internal medicine Specialties of internal medicine Myra E. Woodworth-Hobbs verfasserin aut Jennifer L. Gooch verfasserin aut S. Russ Price verfasserin aut In Kidney Research and Clinical Practice The Korean Society of Nephrology, 2018 31(2012), 2, p A92 (DE-627)689392699 (DE-600)2656420-8 22119140 nnns volume:31 year:2012 number:2, p A92 https://doi.org/10.1016/j.krcp.2012.04.625 kostenfrei https://doaj.org/article/a39ad03fb616440780d7c0ac76fe49cd kostenfrei http://www.sciencedirect.com/science/article/pii/S2211913212006584 kostenfrei https://doaj.org/toc/2211-9132 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_2014 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 31 2012 2, p A92
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source	In Kidney Research and Clinical Practice 31(2012), 2, p A92 volume:31 year:2012 number:2, p A92
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callnumber-first	R - Medicine
author	Matthew B. Hudson
spellingShingle	Matthew B. Hudson misc RC31-1245 misc RC581-951 misc Internal medicine misc Specialties of internal medicine Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
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topic_title	RC31-1245 RC581-951 Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
topic	misc RC31-1245 misc RC581-951 misc Internal medicine misc Specialties of internal medicine
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title	Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
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title_full	Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
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title_sort	calcineurin-nfat signaling regulates atrogin-1 and murf1 via microrna-23a (mir-23a) during muscle atrophy
callnumber	RC31-1245
title_auth	Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
abstract	Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020
abstractGer	Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020
abstract_unstemmed	Muscle atrophy is prevalent in chronic kidney disease (CKD) patients. MicroRNAs play a critical role in biological processes including muscle atrophy. MicroRNA-23a (miR-23a) negatively regulates the expression of two atrophy-related ubiquitin ligases, atrogin-1 and MuRF1; it is reduced in muscle during atrophy. Although miR-23a expression was recently shown to be positively regulated by NFATc3, the underlying mechanism of miR-23a suppression during atrophy remains unknown. We previously reported that the activity of calcineurin (Cn), the calcium-activated phosphatase that regulates NFATc proteins, is decreased when insulin signaling is decreased. Since CKD causes muscle atrophy, and glucocorticoids are required for the response, we investigated how dexamethasone (DEX) affects Cn activity, NFATc3 signaling, and miR-23a expression. C2C12 or L6 myotubes were treated with 100 uM DEX to induce atrophy. Within 1 h, Cn activity was reduced and less NFATc3 was located in the nucleus. Further, miR-23a was also decreased within 30 minutes. After 48 h, expression of the NFATC3 target gene, MCIP1.4, and miR-23a were decreased. Expression of atrogin-1 and MuRF1 were also increased 48 h after DEX. Collectively, these findings indicate the Cn-NFAT signaling pathway may play an important role in the regulation of atrogin-1 and MuRF1 by suppressing miR23a during CKD and glucocorticoid-related muscle atrophy. Support: NIH DK007656; AHA GRNT7660020
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title_short	Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy
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Calcineurin-NFAT signaling regulates atrogin-1 and MuRF1 via microRNA-23a (miR-23a) during muscle atrophy

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