Depletion of CD206+ M2-like macrophages induces fibro-adipogenic progenitors activation and muscle regeneration

Allah Nawaz (), Muhammad Bilal, Shiho Fujisaka, Tomonobu Kado (), Muhammad Rahil Aslam, Saeed Ahmed, Keisuke Okabe, Yoshiko Igarashi, Yoshiyuki Watanabe, Takahide Kuwano, Koichi Tsuneyama, Ayumi Nishimura, Yasuhiro Nishida, Seiji Yamamoto, Masakiyo Sasahara, Johji Imura, Hisashi Mori, Martin M. Matzuk, Fujimi Kudo, Ichiro Manabe, Akiyoshi Uezumi, Takashi Nakagawa, Yumiko Oishi and Kazuyuki Tobe ()
Additional contact information
Allah Nawaz: University of Toyama
Muhammad Bilal: University of Toyama
Shiho Fujisaka: University of Toyama
Tomonobu Kado: University of Toyama
Muhammad Rahil Aslam: University of Toyama
Saeed Ahmed: Rawalpindi Medical University
Keisuke Okabe: University of Toyama
Yoshiko Igarashi: University of Toyama
Yoshiyuki Watanabe: University of Toyama
Takahide Kuwano: University of Toyama
Koichi Tsuneyama: Tokushima University Graduate School
Ayumi Nishimura: University of Toyama
Yasuhiro Nishida: University of Toyama
Seiji Yamamoto: University of Toyama
Masakiyo Sasahara: University of Toyama
Johji Imura: University of Toyama
Hisashi Mori: University of Toyama
Martin M. Matzuk: Baylor College of Medicine
Fujimi Kudo: Chiba University Graduate School of Medicine
Ichiro Manabe: Chiba University Graduate School of Medicine
Akiyoshi Uezumi: Tokushima University
Takashi Nakagawa: University of Toyama
Yumiko Oishi: Nippon Medical School
Kazuyuki Tobe: University of Toyama

Nature Communications, 2022, vol. 13, issue 1, 1-12

Abstract: 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.

Date: 2022
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DOI: 10.1038/s41467-022-34191-y

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