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miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR

microRNAs negatively regulate gene expression by blocking translation or increasing mRNA degradation. In skeletal muscle, these molecules play important roles in adaptive responses, and ongoing investigations are necessary to understand the fine-tune regulation of skeletal muscle mass. Herein we sho...

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Autores principales: Alves, Paula Ketilly Nascimento, Cruz, André, Silva, William J., Labeit, Siegfried, Moriscot, Anselmo Sigari
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9266809/
https://www.ncbi.nlm.nih.gov/pubmed/35806204
http://dx.doi.org/10.3390/ijms23137198
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author Alves, Paula Ketilly Nascimento
Cruz, André
Silva, William J.
Labeit, Siegfried
Moriscot, Anselmo Sigari
author_facet Alves, Paula Ketilly Nascimento
Cruz, André
Silva, William J.
Labeit, Siegfried
Moriscot, Anselmo Sigari
author_sort Alves, Paula Ketilly Nascimento
collection PubMed
description microRNAs negatively regulate gene expression by blocking translation or increasing mRNA degradation. In skeletal muscle, these molecules play important roles in adaptive responses, and ongoing investigations are necessary to understand the fine-tune regulation of skeletal muscle mass. Herein we showed that skeletal muscle overexpression of miR-29c increased fiber size and force at 7 and 30 days after electrotransfer. At both time points, AKT/mTOR pathway components were downregulated, and, surprisingly, overall protein synthesis was strongly elevated at day 7, which normalized by day 30 after pCMVmiR-29c electrotransfer. These results indicate that miR-29c expression induces skeletal muscle hypertrophy and gain of function, which involves increased overall protein synthesis in spite of the deactivation of the AKT/mTOR pathway.
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spelling pubmed-92668092022-07-09 miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR Alves, Paula Ketilly Nascimento Cruz, André Silva, William J. Labeit, Siegfried Moriscot, Anselmo Sigari Int J Mol Sci Communication microRNAs negatively regulate gene expression by blocking translation or increasing mRNA degradation. In skeletal muscle, these molecules play important roles in adaptive responses, and ongoing investigations are necessary to understand the fine-tune regulation of skeletal muscle mass. Herein we showed that skeletal muscle overexpression of miR-29c increased fiber size and force at 7 and 30 days after electrotransfer. At both time points, AKT/mTOR pathway components were downregulated, and, surprisingly, overall protein synthesis was strongly elevated at day 7, which normalized by day 30 after pCMVmiR-29c electrotransfer. These results indicate that miR-29c expression induces skeletal muscle hypertrophy and gain of function, which involves increased overall protein synthesis in spite of the deactivation of the AKT/mTOR pathway. MDPI 2022-06-28 /pmc/articles/PMC9266809/ /pubmed/35806204 http://dx.doi.org/10.3390/ijms23137198 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Communication
Alves, Paula Ketilly Nascimento
Cruz, André
Silva, William J.
Labeit, Siegfried
Moriscot, Anselmo Sigari
miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title_full miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title_fullStr miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title_full_unstemmed miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title_short miR-29c Increases Protein Synthesis in Skeletal Muscle Independently of AKT/mTOR
title_sort mir-29c increases protein synthesis in skeletal muscle independently of akt/mtor
topic Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9266809/
https://www.ncbi.nlm.nih.gov/pubmed/35806204
http://dx.doi.org/10.3390/ijms23137198
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