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程序性细胞死亡蛋白-1 通过调节调节性 T 细胞和巨噬细胞促进挫伤骨骼肌再生。

Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages.

机构信息

School of Kinesiology, Shanghai University of Sport, Shanghai, China.

出版信息

Lab Invest. 2021 Jun;101(6):719-732. doi: 10.1038/s41374-021-00542-4. Epub 2021 Mar 5.

DOI:10.1038/s41374-021-00542-4
PMID:33674785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8137453/
Abstract

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.

摘要

免疫细胞参与骨骼肌再生。调节性 T 细胞(Treg 细胞)参与受损骨骼肌再生的机制尚不清楚。本研究旨在探讨程序性死亡受体 1(PD-1)在挫伤性骨骼肌再生中的作用,并阐明 PD-1 对 Treg 细胞生成和巨噬细胞极化的调节作用,以期加深对免疫系统与受损骨骼肌再生之间关系的理解。结果表明,与野生型小鼠相比,PD-1 敲低减少了 Treg 细胞的数量,并损害了挫伤性骨骼肌的再生。程序性死亡受体 1 基因敲除小鼠挫伤骨骼肌中促炎巨噬细胞的数量增加,促炎因子和氧化应激因子的表达增加,而抗炎巨噬细胞的数量以及抗炎因子、抗氧化应激因子和与肌肉再生相关的因子的表达减少。这些结果表明,PD-1 可以通过调节 Treg 细胞生成和巨噬细胞极化来促进挫伤性骨骼肌再生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/5a7e51d21cf8/41374_2021_542_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/2d686210b0ae/41374_2021_542_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/130b103445b9/41374_2021_542_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/5bcd2c1532c5/41374_2021_542_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/05e31aaf09cb/41374_2021_542_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/c2de48d703cc/41374_2021_542_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/d27290ae30a0/41374_2021_542_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/5a7e51d21cf8/41374_2021_542_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/2d686210b0ae/41374_2021_542_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/7d899c8619a4/41374_2021_542_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/130b103445b9/41374_2021_542_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/5bcd2c1532c5/41374_2021_542_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/05e31aaf09cb/41374_2021_542_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/c2de48d703cc/41374_2021_542_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/d27290ae30a0/41374_2021_542_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69ae/8137453/5a7e51d21cf8/41374_2021_542_Fig8_HTML.jpg

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