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

2021 ◽  
Author(s):  
Jian Shou ◽  
Xinjuan Shi ◽  
Xiaoguang Liu ◽  
Yingjie Chen ◽  
Peijie Chen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Macrophage Polarization ◽  
Treg Cells ◽  
Stress Factors ◽  
Skeletal Muscle Regeneration ◽  
Inflammatory Factors ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Inflammatory Macrophages

AbstractImmune 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.

scholarly journals The Role of Metabolic Remodeling in Macrophage Polarization and Its Effect on Skeletal Muscle Regeneration

2019 ◽  
Vol 30 (12) ◽  
pp. 1553-1598 ◽  
Author(s):  
Francesca De Santa ◽  
Laura Vitiello ◽  
Alessio Torcinaro ◽  
Elisabetta Ferraro
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Macrophage Polarization ◽  
Skeletal Muscle Regeneration ◽  
Metabolic Remodeling

scholarly journals Harnessing Inorganic Nanoparticles to Direct Macrophage Polarization for Skeletal Muscle Regeneration

Nanomaterials ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1963
Author(s):  
Francesca Corsi ◽  
Felicia Carotenuto ◽  
Paolo Di Nardo ◽  
Laura Teodori
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Macrophage Polarization ◽  
Inorganic Nanoparticles ◽  
Skeletal Muscle Regeneration ◽  
Full Potential ◽  
Significant Progress ◽  
Synthetic Scaffolds ◽  
Macrophage Plasticity ◽  
Biomedical Field

Modulation of macrophage plasticity is emerging as a successful strategy in tissue engineering (TE) to control the immune response elicited by the implanted material. Indeed, one major determinant of success in regenerating tissues and organs is to achieve the correct balance between immune pro-inflammatory and pro-resolution players. In recent years, nanoparticle-mediated macrophage polarization towards the pro- or anti-inflammatory subtypes is gaining increasing interest in the biomedical field. In TE, despite significant progress in the use of nanomaterials, the full potential of nanoparticles as effective immunomodulators has not yet been completely realized. This work discusses the contribution that nanotechnology gives to TE applications, helping native or synthetic scaffolds to direct macrophage polarization; here, three bioactive metallic and ceramic nanoparticles (gold, titanium oxide, and cerium oxide nanoparticles) are proposed as potential valuable tools to trigger skeletal muscle regeneration.

scholarly journals Treg cells limit IFN-γ production to control macrophage accrual and phenotype during skeletal muscle regeneration

2018 ◽  
Vol 115 (11) ◽  
pp. E2585-E2593 ◽  
Author(s):  
Marisella Panduro ◽  
Christophe Benoist ◽  
Diane Mathis
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Cell Types ◽  
Treg Cells ◽  
Regenerative Process ◽  
Skeletal Muscle Regeneration ◽  
Acute Injury ◽  
Immune System Cell ◽  
Ifn Γ ◽  
The Impact

Skeletal muscle regeneration is a highly orchestrated process that depends on multiple immune-system cell types, notably macrophages (MFs) and Foxp3+CD4+ regulatory T (Treg) cells. This study addressed how Treg cells rein in MFs during regeneration of murine muscle after acute injury with cardiotoxin. We first delineated and characterized two subsets of MFs according to their expression of major histocompatibility complex class II (MHCII) molecules, i.e., their ability to present antigens. Then, we assessed the impact of Treg cells on these MF subsets by punctually depleting Foxp3+ cells during the regenerative process. Treg cells controlled both the accumulation and phenotype of the two types of MFs. Their absence after injury promoted IFN-γ production, primarily by NK and effector T cells, which ultimately resulted in MF dysregulation and increased inflammation and fibrosis, pointing to compromised muscle repair. Thus, we uncovered an IFN-γ–centered regulatory layer by which Treg cells keep MFs in check and dampen inflammation during regeneration of skeletal muscle.

scholarly journals MicroRNA-223-3p promotes skeletal muscle regeneration by regulating inflammation in mice

2020 ◽  
Vol 295 (30) ◽  
pp. 10212-10223 ◽  
Author(s):  
Naixuan Cheng ◽  
Chang Liu ◽  
Yulin Li ◽  
Shijuan Gao ◽  
Ying-Chun Han ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Molecular Mechanisms ◽  
Interstitial Fibrosis ◽  
Early Stage ◽  
Skeletal Muscle Regeneration ◽  
Inflammatory Factors ◽  
Regeneration Ability ◽  
Macrophage Phenotype ◽  
Anti Inflammatory

After injury, the coordinated balance of pro- and anti-inflammatory factors in the microenvironment contribute to skeletal muscle regeneration. However, the underlying molecular mechanisms regulating this balance remain incompletely understood. In this study, we examined the roles of microRNAs (miRNAs) in inflammation and muscle regeneration. miRNA-Seq transcriptome analysis of mouse skeletal muscle revealed that miR-223-3p is upregulated in the early stage of muscle regeneration after injury. miR-223-3p knockout resulted in increased inflammation, impaired muscle regeneration, and increased interstitial fibrosis. Mechanistically, we found that myeloid-derived miR-223-3p suppresses the target gene interleukin-6 (Il6), associated with the maintenance of the proinflammatory macrophage phenotype during injury. Administration of IL-6-neutralizing antibody in miR-223-3p-knockout muscle could rescue the impaired regeneration ability and reduce the fibrosis. Together, our results reveal that miR-223-3p improves muscle regeneration by regulating inflammation, indicating that miRNAs can participate in skeletal muscle regeneration by controlling the balance of pro- and anti-inflammatory factors in the skeletal muscle microenvironment.

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