MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation

Abstract Thioredoxin reductase 1 (TrxR1) is a selenocysteine-containing protein involved in cellular redox homeostasis which is downregulated in skeletal muscle differentiation. Here we show that TrxR1 decrease occurring during myogenesis is functionally involved in the coordination of this cellular...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Neri Mercatelli, Simona Fittipaldi, Elisa De Paola, Ivan Dimauro, Maria Paola Paronetto, Malcolm J. Jackson, Daniela Caporossi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e645bc62313547519881e1edcaed310b
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:e645bc62313547519881e1edcaed310b
record_format	dspace
spelling	oai:doaj.org-article:e645bc62313547519881e1edcaed310b2021-12-02T12:32:59ZMiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation10.1038/s41598-017-07575-02045-2322https://doaj.org/article/e645bc62313547519881e1edcaed310b2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07575-0https://doaj.org/toc/2045-2322Abstract Thioredoxin reductase 1 (TrxR1) is a selenocysteine-containing protein involved in cellular redox homeostasis which is downregulated in skeletal muscle differentiation. Here we show that TrxR1 decrease occurring during myogenesis is functionally involved in the coordination of this cellular process. Indeed, TrxR1 depletion reduces myoblasts growth by inducing an early myogenesis -related gene expression pattern which includes myogenin and Myf5 up-regulation and Cyclin D1 decrease. On the contrary, the overexpression of TrxR1 during differentiation delays myogenic process, by negatively affecting the expression of Myogenin and MyHC. Moreover, we found that miR-23a and miR-23b - whose expression was increased in the early stage of C2C12 differentiation - are involved in the regulation of TrxR1 expression through their direct binding to the 3′ UTR of TrxR1 mRNA. Interestingly, the forced inhibition of miR-23a and miR-23b during C2C12 differentiation partially rescues TrxR1 levels and delays the expression of myogenic markers, suggesting the involvement of miR-23 in myogenesis via TrxR1 repression. Taken together, our results depict for the first time a novel molecular axis, which functionally acts in skeletal muscle differentiation through the modulation of TrxR1 by miR-23.Neri MercatelliSimona FittipaldiElisa De PaolaIvan DimauroMaria Paola ParonettoMalcolm J. JacksonDaniela CaporossiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Neri Mercatelli Simona Fittipaldi Elisa De Paola Ivan Dimauro Maria Paola Paronetto Malcolm J. Jackson Daniela Caporossi MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
description	Abstract Thioredoxin reductase 1 (TrxR1) is a selenocysteine-containing protein involved in cellular redox homeostasis which is downregulated in skeletal muscle differentiation. Here we show that TrxR1 decrease occurring during myogenesis is functionally involved in the coordination of this cellular process. Indeed, TrxR1 depletion reduces myoblasts growth by inducing an early myogenesis -related gene expression pattern which includes myogenin and Myf5 up-regulation and Cyclin D1 decrease. On the contrary, the overexpression of TrxR1 during differentiation delays myogenic process, by negatively affecting the expression of Myogenin and MyHC. Moreover, we found that miR-23a and miR-23b - whose expression was increased in the early stage of C2C12 differentiation - are involved in the regulation of TrxR1 expression through their direct binding to the 3′ UTR of TrxR1 mRNA. Interestingly, the forced inhibition of miR-23a and miR-23b during C2C12 differentiation partially rescues TrxR1 levels and delays the expression of myogenic markers, suggesting the involvement of miR-23 in myogenesis via TrxR1 repression. Taken together, our results depict for the first time a novel molecular axis, which functionally acts in skeletal muscle differentiation through the modulation of TrxR1 by miR-23.
format	article
author	Neri Mercatelli Simona Fittipaldi Elisa De Paola Ivan Dimauro Maria Paola Paronetto Malcolm J. Jackson Daniela Caporossi
author_facet	Neri Mercatelli Simona Fittipaldi Elisa De Paola Ivan Dimauro Maria Paola Paronetto Malcolm J. Jackson Daniela Caporossi
author_sort	Neri Mercatelli
title	MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
title_short	MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
title_full	MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
title_fullStr	MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
title_full_unstemmed	MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation
title_sort	mir-23-trxr1 as a novel molecular axis in skeletal muscle differentiation
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/e645bc62313547519881e1edcaed310b
work_keys_str_mv	AT nerimercatelli mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT simonafittipaldi mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT elisadepaola mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT ivandimauro mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT mariapaolaparonetto mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT malcolmjjackson mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation AT danielacaporossi mir23trxr1asanovelmolecularaxisinskeletalmuscledifferentiation
_version_	1718393952345784320

MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation

Ejemplares similares