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Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages
Immune cells are involved in skeletal muscle regeneration. The mechanism by which Treg cells are involved in the regeneration of injured skeletal muscle is still unclear. The purpose of this study was to explore the role of programmed death-1 in contused skeletal muscle regeneration, and to clarify...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group US
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8137453/ https://www.ncbi.nlm.nih.gov/pubmed/33674785 http://dx.doi.org/10.1038/s41374-021-00542-4 |
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author | Shou, Jian Shi, Xinjuan Liu, Xiaoguang Chen, Yingjie Chen, Peijie Xiao, Weihua |
author_facet | Shou, Jian Shi, Xinjuan Liu, Xiaoguang Chen, Yingjie Chen, Peijie Xiao, Weihua |
author_sort | Shou, Jian |
collection | PubMed |
description | Immune cells are involved in skeletal muscle regeneration. The mechanism by which Treg cells are involved in the regeneration of injured skeletal muscle is still unclear. The purpose of this study was to explore the role of programmed death-1 in contused skeletal muscle regeneration, and to clarify the regulation of programmed death-1 on Treg cell generation and macrophage polarization, in order to deepen our understanding of the relationship between the immune system and injured skeletal muscle regeneration. The results show that programmed death-1 knockdown reduced the number of Treg cells and impaired contused skeletal muscle regeneration compared with those of wild-type mice. The number of pro-inflammatory macrophages in the contused skeletal muscle of programmed death-1 knockout mice increased, and the expression of pro-inflammatory factors and oxidative stress factors increased, while the number of anti-inflammatory macrophages and the expression of anti-inflammatory factors, antioxidant stress factors, and muscle regeneration-related factors decreased. These results suggest that programmed death-1 can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization. |
format | Online Article Text |
id | pubmed-8137453 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group US |
record_format | MEDLINE/PubMed |
spelling | pubmed-81374532021-06-03 Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages Shou, Jian Shi, Xinjuan Liu, Xiaoguang Chen, Yingjie Chen, Peijie Xiao, Weihua Lab Invest Article Immune cells are involved in skeletal muscle regeneration. The mechanism by which Treg cells are involved in the regeneration of injured skeletal muscle is still unclear. The purpose of this study was to explore the role of programmed death-1 in contused skeletal muscle regeneration, and to clarify the regulation of programmed death-1 on Treg cell generation and macrophage polarization, in order to deepen our understanding of the relationship between the immune system and injured skeletal muscle regeneration. The results show that programmed death-1 knockdown reduced the number of Treg cells and impaired contused skeletal muscle regeneration compared with those of wild-type mice. The number of pro-inflammatory macrophages in the contused skeletal muscle of programmed death-1 knockout mice increased, and the expression of pro-inflammatory factors and oxidative stress factors increased, while the number of anti-inflammatory macrophages and the expression of anti-inflammatory factors, antioxidant stress factors, and muscle regeneration-related factors decreased. These results suggest that programmed death-1 can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization. Nature Publishing Group US 2021-03-05 2021 /pmc/articles/PMC8137453/ /pubmed/33674785 http://dx.doi.org/10.1038/s41374-021-00542-4 Text en © The Author(s), under exclusive licence to United States and Canadian Academy of Pathology 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Shou, Jian Shi, Xinjuan Liu, Xiaoguang Chen, Yingjie Chen, Peijie Xiao, Weihua Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title | Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title_full | Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title_fullStr | Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title_full_unstemmed | Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title_short | Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages |
title_sort | programmed death-1 promotes contused skeletal muscle regeneration by regulating treg cells and macrophages |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8137453/ https://www.ncbi.nlm.nih.gov/pubmed/33674785 http://dx.doi.org/10.1038/s41374-021-00542-4 |
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