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- Title
Depletion of CD206<sup>+</sup> M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration.
- Authors
Nawaz, Allah; Bilal, Muhammad; Fujisaka, Shiho; Kado, Tomonobu; Aslam, Muhammad Rahil; Ahmed, Saeed; Okabe, Keisuke; Igarashi, Yoshiko; Watanabe, Yoshiyuki; Kuwano, Takahide; Tsuneyama, Koichi; Nishimura, Ayumi; Nishida, Yasuhiro; Yamamoto, Seiji; Sasahara, Masakiyo; Imura, Johji; Mori, Hisashi; Matzuk, Martin M.; Kudo, Fujimi; Manabe, Ichiro
- 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. Muscle regeneration requires the contribution and communication of various different cell types. Here, Nawaz et al. show that CD206+ macrophages inhibit the secretion of the promyogenic factor follistatin by fibro-adipogenic progenitor cells, impeding myogenesis and muscle regeneration.
- Subjects
SATELLITE cells; PROGENITOR cells; CELL physiology; STEM cells; MUSCLE cells; MUSCLE regeneration; MACROPHAGES
- Publication
Nature Communications, 2022, Vol 13, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-022-34191-y