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Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo

Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the prese...

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Autores principales: Lei, Si, She, Yanling, Zeng, Jie, Chen, Rui, Zhou, Shanyao, Shi, Huacai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6798001/
https://www.ncbi.nlm.nih.gov/pubmed/31545487
http://dx.doi.org/10.3892/mmr.2019.10661
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author Lei, Si
She, Yanling
Zeng, Jie
Chen, Rui
Zhou, Shanyao
Shi, Huacai
author_facet Lei, Si
She, Yanling
Zeng, Jie
Chen, Rui
Zhou, Shanyao
Shi, Huacai
author_sort Lei, Si
collection PubMed
description Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin-1 were increased, both in vitro and in vivo. The impact of starvation on the expression patterns of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) was next determined. The expression patterns of miR-23a, miR-206 and miR-27b in the starved mice exhibited similar trends as those in starved C2C12 cells in vitro, whereas the expression patterns of six other miRNAs (miR-18a, miR-133a, miR-133b, miR-186, miR-1a and miR-29b) differed between the in vivo and the in vitro starvation models. The present study indicated that in vitro expression of the selected miRNAs was not completely consistent with that in vivo. By contrast, lncRNAs showed excellent consistency in their expression patterns in both the in vitro and in vivo starvation models; six of the lncRNAs (Atrolnc-1, long intergenic non-protein coding RNA of muscle differentiation 1, Myolinc, lncRNA myogenic differentiation 1, Dum and muscle anabolic regulator 1) were significantly elevated in starved tissues and cells, while lnc-mg was significantly decreased, compared with the control groups. Thus, lncRNAs involved in muscle atrophy have the potential to be developed as diagnostic tools.
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spelling pubmed-67980012019-10-22 Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo Lei, Si She, Yanling Zeng, Jie Chen, Rui Zhou, Shanyao Shi, Huacai Mol Med Rep Articles Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin-1 were increased, both in vitro and in vivo. The impact of starvation on the expression patterns of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) was next determined. The expression patterns of miR-23a, miR-206 and miR-27b in the starved mice exhibited similar trends as those in starved C2C12 cells in vitro, whereas the expression patterns of six other miRNAs (miR-18a, miR-133a, miR-133b, miR-186, miR-1a and miR-29b) differed between the in vivo and the in vitro starvation models. The present study indicated that in vitro expression of the selected miRNAs was not completely consistent with that in vivo. By contrast, lncRNAs showed excellent consistency in their expression patterns in both the in vitro and in vivo starvation models; six of the lncRNAs (Atrolnc-1, long intergenic non-protein coding RNA of muscle differentiation 1, Myolinc, lncRNA myogenic differentiation 1, Dum and muscle anabolic regulator 1) were significantly elevated in starved tissues and cells, while lnc-mg was significantly decreased, compared with the control groups. Thus, lncRNAs involved in muscle atrophy have the potential to be developed as diagnostic tools. D.A. Spandidos 2019-11 2019-09-10 /pmc/articles/PMC6798001/ /pubmed/31545487 http://dx.doi.org/10.3892/mmr.2019.10661 Text en Copyright: © Lei et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lei, Si
She, Yanling
Zeng, Jie
Chen, Rui
Zhou, Shanyao
Shi, Huacai
Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title_full Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title_fullStr Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title_full_unstemmed Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title_short Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo
title_sort expression patterns of regulatory lncrnas and mirnas in muscular atrophy models induced by starvation in vitro and in vivo
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6798001/
https://www.ncbi.nlm.nih.gov/pubmed/31545487
http://dx.doi.org/10.3892/mmr.2019.10661
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