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LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1
BACKGROUND: H19 is a well-characterized Long noncoding RNA (lncRNA) that has been proven to promote myoblast differentiation in humans and mice. However, its mechanism of action is still not fully interpreted. METHODS: Using RT-qPCR, we examined H19 RNA levels in various tissues from 1-week, 1-month...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481879/ https://www.ncbi.nlm.nih.gov/pubmed/28652859 http://dx.doi.org/10.1186/s11658-017-0040-6 |
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author | Xu, Xiaochun Ji, Shengyue Li, Weili Yi, Bao Li, Hengxin Zhang, Hongfu Ma, Wenping |
author_facet | Xu, Xiaochun Ji, Shengyue Li, Weili Yi, Bao Li, Hengxin Zhang, Hongfu Ma, Wenping |
author_sort | Xu, Xiaochun |
collection | PubMed |
description | BACKGROUND: H19 is a well-characterized Long noncoding RNA (lncRNA) that has been proven to promote myoblast differentiation in humans and mice. However, its mechanism of action is still not fully interpreted. METHODS: Using RT-qPCR, we examined H19 RNA levels in various tissues from 1-week, 1-month, 6-month and 36-month old male cattle (i.e., newborn, infant, young and adult). The protein and mRNA levels of MyoG, MyHC, Sirt1 and FoxO1 in the satellite and C(2)C(12) cells with an H19 silencing or overexpression vector were respectively detected using western blot and real-time qPCR. RESULTS: H19 was highly expressed in skeletal muscle at all the studied ages. High expression of H19 was required for the differentiation of bovine satellite cells. Knockdown of H19 caused a remarkable increase in the myoblast-inhibitory genes Sirt1/FoxO1, suggesting that H19 suppresses Sirt1/FoxO1 expression during myogenesis. Western blotting analysis of co-transfection of Sirt1 or FoxO1 expression vectors with pcDNA-H19 indicated that Sirt1/FoxO1 overexpression neutralized the promotion of myoblast differentiation through transfection of pcDNA-H19. CONCLUSION: H19 promoted the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s11658-017-0040-6) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5481879 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-54818792017-06-26 LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 Xu, Xiaochun Ji, Shengyue Li, Weili Yi, Bao Li, Hengxin Zhang, Hongfu Ma, Wenping Cell Mol Biol Lett Short Report BACKGROUND: H19 is a well-characterized Long noncoding RNA (lncRNA) that has been proven to promote myoblast differentiation in humans and mice. However, its mechanism of action is still not fully interpreted. METHODS: Using RT-qPCR, we examined H19 RNA levels in various tissues from 1-week, 1-month, 6-month and 36-month old male cattle (i.e., newborn, infant, young and adult). The protein and mRNA levels of MyoG, MyHC, Sirt1 and FoxO1 in the satellite and C(2)C(12) cells with an H19 silencing or overexpression vector were respectively detected using western blot and real-time qPCR. RESULTS: H19 was highly expressed in skeletal muscle at all the studied ages. High expression of H19 was required for the differentiation of bovine satellite cells. Knockdown of H19 caused a remarkable increase in the myoblast-inhibitory genes Sirt1/FoxO1, suggesting that H19 suppresses Sirt1/FoxO1 expression during myogenesis. Western blotting analysis of co-transfection of Sirt1 or FoxO1 expression vectors with pcDNA-H19 indicated that Sirt1/FoxO1 overexpression neutralized the promotion of myoblast differentiation through transfection of pcDNA-H19. CONCLUSION: H19 promoted the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s11658-017-0040-6) contains supplementary material, which is available to authorized users. BioMed Central 2017-06-23 /pmc/articles/PMC5481879/ /pubmed/28652859 http://dx.doi.org/10.1186/s11658-017-0040-6 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Short Report Xu, Xiaochun Ji, Shengyue Li, Weili Yi, Bao Li, Hengxin Zhang, Hongfu Ma, Wenping LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title | LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title_full | LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title_fullStr | LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title_full_unstemmed | LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title_short | LncRNA H19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing Sirt1/FoxO1 |
title_sort | lncrna h19 promotes the differentiation of bovine skeletal muscle satellite cells by suppressing sirt1/foxo1 |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481879/ https://www.ncbi.nlm.nih.gov/pubmed/28652859 http://dx.doi.org/10.1186/s11658-017-0040-6 |
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