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C-MAF defines the phenotype of a family of perivascular macrophages

ABSTRACT: Tissue-resident Macrophages have long been appreciated as playing a fundamental role in the ontogeny and function of several organs. For example, osteoclasts are crucial for proper bone remodeling, microglia for synaptic pruning, and lung alveolar macrophages for clearance of surfactant. Perivascular macrophages have been described in many organs. Our analysis of murine perivascular macrophages in several tissues and organs led us to define a macrophage family, whose members share the expression of a number of surface molecules that are not typically considered macrophage markers, such as Lyve1, Folate Receptor 2 (Folr2), Enpep/CD249, and CD38, as well as other more typical macrophage markers such as CD206 and Tim4. This family of perivascular macrophages also occurs in humans. Importantly, this family of perivascular macrophages relies on the transcription factor c-MAF, encoded by the gene Maf, for its full function. Conditional deletion of the Maf gene in the Lyve1+Folr2+CD38+ macrophage family caused their ablation in the brain, without impact on the microglia, while in the adipose tissue the conditional deletion of the Maf gene in perivascular macrophages resulted in a profoundly altered macrophage gene expression, and brought about an increased vascular branching in this tissue. Mice with conditional Maf deletion were protected from metabolic syndrome when submitted to high fat diet (HFD). Our results show that c-MAF is the master regulator of a family of perivascular macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE148606 | GEO | 2021/09/30

REPOSITORIES: GEO

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c-MAF defines the phenotype of a family of perivascular macrophages

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| PRJNA625192 | ENA

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