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miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy

Skeletal muscle atrophy is a complex degenerative disease characterized by decreased skeletal muscle mass, skeletal muscle strength, and function. MicroRNAs (miRNAs) are a potential therapeutic target, and natural products that regulate miRNA expression may be a safe and effective treatment strategy...

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Detalles Bibliográficos
Autores principales: Gan, Mailin, Ma, Jianfeng, Chen, Jingyun, Chen, Lei, Zhang, Shunhua, Zhao, Ye, Niu, Lili, Li, Xuewei, Zhu, Li, Shen, Linyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9104324/
https://www.ncbi.nlm.nih.gov/pubmed/35565830
http://dx.doi.org/10.3390/nu14091861
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author Gan, Mailin
Ma, Jianfeng
Chen, Jingyun
Chen, Lei
Zhang, Shunhua
Zhao, Ye
Niu, Lili
Li, Xuewei
Zhu, Li
Shen, Linyuan
author_facet Gan, Mailin
Ma, Jianfeng
Chen, Jingyun
Chen, Lei
Zhang, Shunhua
Zhao, Ye
Niu, Lili
Li, Xuewei
Zhu, Li
Shen, Linyuan
author_sort Gan, Mailin
collection PubMed
description Skeletal muscle atrophy is a complex degenerative disease characterized by decreased skeletal muscle mass, skeletal muscle strength, and function. MicroRNAs (miRNAs) are a potential therapeutic target, and natural products that regulate miRNA expression may be a safe and effective treatment strategy for muscle atrophy. Previous studies have shown beneficial effects of genistein treatment on muscle mass and muscle atrophy, but the mechanism is not fully understood. Differential co-expression network analysis revealed that miR-222 was upregulated in multiple skeletal muscle atrophy models. Subsequent in vitro (C2C12 myoblasts) and in vivo (C57BL/6 mice) experiments showed that genistein could alleviate dexamethasone-induced muscle atrophy and downregulate the expression of miR-222 in muscle tissue and C2C12 myotubes. The dual-luciferase reporter assay system confirmed that IGF1 is a target gene of miR-222 and is regulated by genistein. In C2C12 myotubes, both dexamethasone and miR-222 overexpression promoted muscle atrophy, however, this function was significantly reduced after genistein treatment. Furthermore, we also observed that both genistein and miR-222 antagomiR could significantly inhibit dexamethasone-induced muscle atrophy in vivo. These results suggest that miR-222 may be involved in the regulation of genistein on muscle atrophy, and genistein and miR-222 may be used to improve muscle health.
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spelling pubmed-91043242022-05-14 miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy Gan, Mailin Ma, Jianfeng Chen, Jingyun Chen, Lei Zhang, Shunhua Zhao, Ye Niu, Lili Li, Xuewei Zhu, Li Shen, Linyuan Nutrients Article Skeletal muscle atrophy is a complex degenerative disease characterized by decreased skeletal muscle mass, skeletal muscle strength, and function. MicroRNAs (miRNAs) are a potential therapeutic target, and natural products that regulate miRNA expression may be a safe and effective treatment strategy for muscle atrophy. Previous studies have shown beneficial effects of genistein treatment on muscle mass and muscle atrophy, but the mechanism is not fully understood. Differential co-expression network analysis revealed that miR-222 was upregulated in multiple skeletal muscle atrophy models. Subsequent in vitro (C2C12 myoblasts) and in vivo (C57BL/6 mice) experiments showed that genistein could alleviate dexamethasone-induced muscle atrophy and downregulate the expression of miR-222 in muscle tissue and C2C12 myotubes. The dual-luciferase reporter assay system confirmed that IGF1 is a target gene of miR-222 and is regulated by genistein. In C2C12 myotubes, both dexamethasone and miR-222 overexpression promoted muscle atrophy, however, this function was significantly reduced after genistein treatment. Furthermore, we also observed that both genistein and miR-222 antagomiR could significantly inhibit dexamethasone-induced muscle atrophy in vivo. These results suggest that miR-222 may be involved in the regulation of genistein on muscle atrophy, and genistein and miR-222 may be used to improve muscle health. MDPI 2022-04-29 /pmc/articles/PMC9104324/ /pubmed/35565830 http://dx.doi.org/10.3390/nu14091861 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 Article
Gan, Mailin
Ma, Jianfeng
Chen, Jingyun
Chen, Lei
Zhang, Shunhua
Zhao, Ye
Niu, Lili
Li, Xuewei
Zhu, Li
Shen, Linyuan
miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title_full miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title_fullStr miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title_full_unstemmed miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title_short miR-222 Is Involved in the Amelioration Effect of Genistein on Dexamethasone-Induced Skeletal Muscle Atrophy
title_sort mir-222 is involved in the amelioration effect of genistein on dexamethasone-induced skeletal muscle atrophy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9104324/
https://www.ncbi.nlm.nih.gov/pubmed/35565830
http://dx.doi.org/10.3390/nu14091861
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