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miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats
Muscle growth and injury-induced regeneration are controlled by skeletal muscle satellite cells (MuSCs) through myogenesis in postnatal animals. Meanwhile, myogenesis is accompanied by mitochondrial function and enzyme activity. Nevertheless, the underlying molecular mechanisms involving non-coding...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10179409/ https://www.ncbi.nlm.nih.gov/pubmed/37176056 http://dx.doi.org/10.3390/ijms24098341 |
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author | Odame, Emmanuel Li, Li Nabilla, Joshua Abdulai Cai, He Xiao, Miao Ye, Jiangfeng Chen, Yuan Kyei, Bismark Dai, Dinghui Zhan, Siyuan Cao, Jiaxue Guo, Jiazhong Zhong, Tao Wang, Linjie Zhang, Hongping |
author_facet | Odame, Emmanuel Li, Li Nabilla, Joshua Abdulai Cai, He Xiao, Miao Ye, Jiangfeng Chen, Yuan Kyei, Bismark Dai, Dinghui Zhan, Siyuan Cao, Jiaxue Guo, Jiazhong Zhong, Tao Wang, Linjie Zhang, Hongping |
author_sort | Odame, Emmanuel |
collection | PubMed |
description | Muscle growth and injury-induced regeneration are controlled by skeletal muscle satellite cells (MuSCs) through myogenesis in postnatal animals. Meanwhile, myogenesis is accompanied by mitochondrial function and enzyme activity. Nevertheless, the underlying molecular mechanisms involving non-coding RNAs including circular RNAs (circRNAs) and microRNAs (miRNAs) remain largely unsolved. Here, we explored the myogenic roles of miR-145-3p and MYBL1 on muscle development and mitochondrial mass. We noticed that overexpression of miR-145-3p inhibited MuSCs proliferation and reduced the number of viable cells. Meanwhile, deficiency of miR-145-3p caused by LNAantimiR-145-3p or an inhibitor retarded the differentiation of MuSCs. miR-145-3p altered the mitochondrial mass in MuSCs. Moreover, miR-145-3p targeted and negatively regulated the expression of CDR1as and MYBL1. The knockdown of the MYBL1 using ASO-2′MOE modification simulated the inhibitory function of miR-145-3p on cell proliferation. Additionally, MYBL1 mediated the regulation of miR-145-3p on Vexin, VCPIP1, COX1, COX2, and Pax7. These imply that CDR1as/miR-145-3p/MYBL1/COX1, COX2, VCPIP1/Vexin expression at least partly results in a reduction in mitochondrial mass and MuSCs proliferation. These novel findings confirm the importance of mitochondrial mass during myogenesis and the boosting of muscle/meat development in mammals. |
format | Online Article Text |
id | pubmed-10179409 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-101794092023-05-13 miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats Odame, Emmanuel Li, Li Nabilla, Joshua Abdulai Cai, He Xiao, Miao Ye, Jiangfeng Chen, Yuan Kyei, Bismark Dai, Dinghui Zhan, Siyuan Cao, Jiaxue Guo, Jiazhong Zhong, Tao Wang, Linjie Zhang, Hongping Int J Mol Sci Article Muscle growth and injury-induced regeneration are controlled by skeletal muscle satellite cells (MuSCs) through myogenesis in postnatal animals. Meanwhile, myogenesis is accompanied by mitochondrial function and enzyme activity. Nevertheless, the underlying molecular mechanisms involving non-coding RNAs including circular RNAs (circRNAs) and microRNAs (miRNAs) remain largely unsolved. Here, we explored the myogenic roles of miR-145-3p and MYBL1 on muscle development and mitochondrial mass. We noticed that overexpression of miR-145-3p inhibited MuSCs proliferation and reduced the number of viable cells. Meanwhile, deficiency of miR-145-3p caused by LNAantimiR-145-3p or an inhibitor retarded the differentiation of MuSCs. miR-145-3p altered the mitochondrial mass in MuSCs. Moreover, miR-145-3p targeted and negatively regulated the expression of CDR1as and MYBL1. The knockdown of the MYBL1 using ASO-2′MOE modification simulated the inhibitory function of miR-145-3p on cell proliferation. Additionally, MYBL1 mediated the regulation of miR-145-3p on Vexin, VCPIP1, COX1, COX2, and Pax7. These imply that CDR1as/miR-145-3p/MYBL1/COX1, COX2, VCPIP1/Vexin expression at least partly results in a reduction in mitochondrial mass and MuSCs proliferation. These novel findings confirm the importance of mitochondrial mass during myogenesis and the boosting of muscle/meat development in mammals. MDPI 2023-05-06 /pmc/articles/PMC10179409/ /pubmed/37176056 http://dx.doi.org/10.3390/ijms24098341 Text en © 2023 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 | Article Odame, Emmanuel Li, Li Nabilla, Joshua Abdulai Cai, He Xiao, Miao Ye, Jiangfeng Chen, Yuan Kyei, Bismark Dai, Dinghui Zhan, Siyuan Cao, Jiaxue Guo, Jiazhong Zhong, Tao Wang, Linjie Zhang, Hongping miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title | miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title_full | miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title_fullStr | miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title_full_unstemmed | miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title_short | miR-145-3p Inhibits MuSCs Proliferation and Mitochondria Mass via Targeting MYBL1 in Jianzhou Big-Eared Goats |
title_sort | mir-145-3p inhibits muscs proliferation and mitochondria mass via targeting mybl1 in jianzhou big-eared goats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10179409/ https://www.ncbi.nlm.nih.gov/pubmed/37176056 http://dx.doi.org/10.3390/ijms24098341 |
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