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DPPIV+ fibro-adipogenic progenitors form the niche of adult skeletal muscle self-renewing resident macrophages.


ABSTRACT: Adult tissue-resident macrophages (RMs) are either maintained by blood monocytes or through self-renewal. While the presence of a nurturing niche is likely crucial to support the survival and function of self-renewing RMs, evidence regarding its nature is limited. Here, we identify fibro-adipogenic progenitors (FAPs) as the main source of colony-stimulating factor 1 (CSF1) in resting skeletal muscle. Using parabiosis in combination with FAP-deficient transgenic mice (PdgfrαCreERT2 × DTA) or mice lacking FAP-derived CSF1 (PdgfrαCreERT2 × Csf1flox/null), we show that local CSF1 from FAPs is required for the survival of both TIM4- monocyte-derived and TIM4+ self-renewing RMs in adult skeletal muscle. The spatial distribution and number of TIM4+ RMs coincide with those of dipeptidyl peptidase IV (DPPIV)+ FAPs, suggesting their role as CSF1-producing niche cells for self-renewing RMs. This finding identifies opportunities to precisely manipulate the function of self-renewing RMs in situ to further unravel their role in health and disease.

SUBMITTER: Babaeijandaghi F 

PROVIDER: S-EPMC10719395 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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DPPIV<sup>+</sup> fibro-adipogenic progenitors form the niche of adult skeletal muscle self-renewing resident macrophages.

Babaeijandaghi Farshad F   Kajabadi Nasim N   Long Reece R   Tung Lin Wei LW   Cheung Chun Wai CW   Ritso Morten M   Chang Chih-Kai CK   Cheng Ryan R   Huang Tiffany T   Groppa Elena E   Jiang Jean X JX   Rossi Fabio M V FMV  

Nature communications 20231213 1


Adult tissue-resident macrophages (RMs) are either maintained by blood monocytes or through self-renewal. While the presence of a nurturing niche is likely crucial to support the survival and function of self-renewing RMs, evidence regarding its nature is limited. Here, we identify fibro-adipogenic progenitors (FAPs) as the main source of colony-stimulating factor 1 (CSF1) in resting skeletal muscle. Using parabiosis in combination with FAP-deficient transgenic mice (Pdgfrα<sup>CreERT2</sup> × D  ...[more]

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