Language
English
Publication Date
11-21-2022
Journal
Nature Communications
DOI
10.1038/s41467-022-34191-y
PMID
36411280
PMCID
PMC9678897
PubMedCentral® Posted Date
11-21-2022
PubMedCentral® Full Text Version
Post-print
Abstract
Muscle regeneration requires the coordination of muscle stem cells, mesenchymal fibro-adipogenic progenitors (FAPs), and macrophages. How macrophages regulate the paracrine secretion of FAPs during the recovery process remains elusive. Herein, we systemically investigated the communication between CD206+ M2-like macrophages and FAPs during the recovery process using a transgenic mouse model. Depletion of CD206+ M2-like macrophages or deletion of CD206+ M2-like macrophages-specific TGF-β1 gene induces myogenesis and muscle regeneration. We show that depletion of CD206+ M2-like macrophages activates FAPs and activated FAPs secrete follistatin, a promyogenic factor, thereby boosting the recovery process. Conversely, deletion of the FAP-specific follistatin gene results in impaired muscle stem cell function, enhanced fibrosis, and delayed muscle regeneration. Mechanistically, CD206+ M2-like macrophages inhibit the secretion of FAP-derived follistatin via TGF-β signaling. Here we show that CD206+ M2-like macrophages constitute a microenvironment for FAPs and may regulate the myogenic potential of muscle stem/satellite cells.
Keywords
Animals, Mice, Adipogenesis, Follistatin, Macrophages, Mice, Transgenic, Muscles, Mannose Receptor, Monocytes and macrophages, Mesenchymal stem cells
Published Open-Access
yes
Recommended Citation
Nawaz, Allah; Bilal, Muhammad; Fujisaka, Shiho; et al., "Depletion of CD206+ M2-Like Macrophages Induces Fibro-Adipogenic Progenitors Activation and Muscle Regeneration" (2022). Faculty and Staff Publications. 2862.
https://digitalcommons.library.tmc.edu/baylor_docs/2862
Included in
Immunology of Infectious Disease Commons, Immunopathology Commons, Medical Immunology Commons, Pathology Commons