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ID 118935
著者
Nawaz, Allah University of Toyama|Harvard Medical School
Bilal, Muhammad University of Toyama
Fujisaka, Shiho University of Toyama
Kado, Tomonobu University of Toyama
Aslam, Muhammad Rahil University of Toyama
Ahmed, Saeed Rawalpindi Medical University
Okabe, Keisuke University of Toyama
Igarashi, Yoshiko University of Toyama
Watanabe, Yoshiyuki University of Toyama
Kuwano, Takahide University of Toyama
Nishimura, Ayumi University of Toyama
Nishida, Yasuhiro University of Toyama
Yamamoto, Seiji University of Toyama
Sasahara, Masakiyo University of Toyama
Imura, Johji University of Toyama
Mori, Hisashi University of Toyama
Matzuk, Martin M. Baylor College of Medicine
Kudo, Fujimi Chiba University
Manabe, Ichiro Chiba University
Nakagawa, Takashi University of Toyama
Oishi, Yumiko Nippon Medical School
Tobe, Kazuyuki University of Toyama
資料タイプ
学術雑誌論文
抄録
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.
掲載誌名
Nature Communications
ISSN
20411723
cat書誌ID
AA12645905
出版者
Springer Nature
13
開始ページ
7058
発行日
2022-11-21
権利情報
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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言語
eng
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出版社版
部局
医学系