RapamycinFungusV1, Main, Exploration, bibRecord, 000083

MicroRNA-99b-5p downregulates protein synthesis in human primary myotubes.

Identifieur interne : 000083 ( Main/Exploration ); précédent : 000082; suivant : 000084

MicroRNA-99b-5p downregulates protein synthesis in human primary myotubes.

Auteurs : Evelyn Zacharewicz [Australie] ; Ming Kalanon [Australie] ; Robyn M. Murphy [Australie] ; Aaron P. Russell [Australie] ; Séverine Lamon [Australie]

Source :

American journal of physiology. Cell physiology [ 1522-1563 ] ; 2020.

RBID : pubmed:32608991

Descripteurs français

English descriptors

KwdEn :
- 3' Untranslated Regions (genetics), Animals (MeSH), Cell Proliferation (genetics), Gene Expression Regulation (genetics), Humans (MeSH), Mechanistic Target of Rapamycin Complex 1 (genetics), Mice (MeSH), MicroRNAs (genetics), Muscle Fibers, Skeletal (metabolism), Myoblasts (metabolism), Protein Biosynthesis (genetics), Signal Transduction (genetics), TOR Serine-Threonine Kinases (genetics).
MESH :
- chemical , genetics : 3' Untranslated Regions, Mechanistic Target of Rapamycin Complex 1, MicroRNAs, TOR Serine-Threonine Kinases.
- genetics : Cell Proliferation, Gene Expression Regulation, Protein Biosynthesis, Signal Transduction.
- metabolism : Muscle Fibers, Skeletal, Myoblasts.
- Animals, Humans, Mice.

Abstract

microRNAs (miRNAs) are important regulators of cellular homeostasis and exert their effect by directly controlling protein expression. We have previously reported an age-dependent negative association between microRNA-99b (miR-99b-5p) expression and muscle protein synthesis in human muscle in vivo. Here we investigated the role of miR-99b-5p as a potential negative regulator of protein synthesis via inhibition of mammalian target for rapamycin (MTOR) signaling in human primary myocytes. Overexpressing miR-99b-5p in human primary myotubes from young and old subjects significantly decreased protein synthesis with no effect of donor age. A binding interaction between miR-99b-5p and its putative binding site within the MTOR 3'-untranslated region (UTR) was confirmed in C₂C₁₂ myoblasts. The observed decline in protein synthesis was, however, not associated with a suppression of the MTOR protein but of its regulatory associated protein of mTOR complex 1 (RPTOR). These results demonstrate that modulating the expression levels of a miRNA can regulate protein synthesis in human muscle cells and provide a potential mechanism for muscle wasting in vivo.

DOI: 10.1152/ajpcell.00172.2020
PubMed: 32608991

Affiliations:

Australie

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000053
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Le document en format XML

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<term>Gene Expression Regulation (genetics)</term>
<term>Humans (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (genetics)</term>
<term>Mice (MeSH)</term>
<term>MicroRNAs (genetics)</term>
<term>Muscle Fibers, Skeletal (metabolism)</term>
<term>Myoblasts (metabolism)</term>
<term>Protein Biosynthesis (genetics)</term>
<term>Signal Transduction (genetics)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Biosynthèse des protéines (génétique)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (génétique)</term>
<term>Fibres musculaires squelettiques (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Myoblastes (métabolisme)</term>
<term>Prolifération cellulaire (génétique)</term>
<term>Régions 3' non traduites (génétique)</term>
<term>Régulation de l'expression des gènes (génétique)</term>
<term>Souris (MeSH)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Transduction du signal (génétique)</term>
<term>microARN (génétique)</term>
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<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>MicroRNAs</term>
<term>TOR Serine-Threonine Kinases</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Proliferation</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Biosynthèse des protéines</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Prolifération cellulaire</term>
<term>Régions 3' non traduites</term>
<term>Régulation de l'expression des gènes</term>
<term>Sérine-thréonine kinases TOR</term>
<term>Transduction du signal</term>
<term>microARN</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Muscle Fibers, Skeletal</term>
<term>Myoblasts</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Fibres musculaires squelettiques</term>
<term>Myoblastes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Mice</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
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<front><div type="abstract" xml:lang="en">microRNAs (miRNAs) are important regulators of cellular homeostasis and exert their effect by directly controlling protein expression. We have previously reported an age-dependent negative association between microRNA-99b (miR-99b-5p) expression and muscle protein synthesis in human muscle in vivo. Here we investigated the role of miR-99b-5p as a potential negative regulator of protein synthesis via inhibition of mammalian target for rapamycin (MTOR) signaling in human primary myocytes. Overexpressing miR-99b-5p in human primary myotubes from young and old subjects significantly decreased protein synthesis with no effect of donor age. A binding interaction between miR-99b-5p and its putative binding site within the <i>MTOR</i>
 3'-untranslated region (UTR) was confirmed in C<sub>2</sub>
C<sub>12</sub>
 myoblasts. The observed decline in protein synthesis was, however, not associated with a suppression of the MTOR protein but of its regulatory associated protein of mTOR complex 1 (RPTOR). These results demonstrate that modulating the expression levels of a miRNA can regulate protein synthesis in human muscle cells and provide a potential mechanism for muscle wasting in vivo.</div>
</front>
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<Abstract><AbstractText>microRNAs (miRNAs) are important regulators of cellular homeostasis and exert their effect by directly controlling protein expression. We have previously reported an age-dependent negative association between microRNA-99b (miR-99b-5p) expression and muscle protein synthesis in human muscle in vivo. Here we investigated the role of miR-99b-5p as a potential negative regulator of protein synthesis via inhibition of mammalian target for rapamycin (MTOR) signaling in human primary myocytes. Overexpressing miR-99b-5p in human primary myotubes from young and old subjects significantly decreased protein synthesis with no effect of donor age. A binding interaction between miR-99b-5p and its putative binding site within the <i>MTOR</i>
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C<sub>12</sub>
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MicroRNA-99b-5p downregulates protein synthesis in human primary myotubes.

MicroRNA-99b-5p downregulates protein synthesis in human primary myotubes.

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Abstract

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