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Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle

ABSTRACT: The membrane protein Cripto plays a key role in shaping macrophage plasticity in skeletal muscle during regeneration and disease. Cripto acts as an extrinsic modulator of macrophage plasticity and is required for the proper expansion/maintenance of the CD206+ anti-inflammatory macrophage population. Nevertheless, Cripto deletion does not change the gene expression profile of F4/80+/Ly6CLow macrophages suggesting that Cripto was dispensable to induce/maintain the Ly6CLow phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE142072 | GEO | 2020/02/06

REPOSITORIES: GEO

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Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle

Project description:Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle

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Cripto shapes macrophage plasticity and restricts EndMT in injured and diseased skeletal muscle.

Project description:Macrophages are characterized by a high plasticity in response to changes in tissue microenvironment, which allows them to acquire different phenotypes and to exert essential functions in complex processes, such as tissue regeneration. Here, we report that the membrane protein Cripto plays a key role in shaping macrophage plasticity in skeletal muscle during regeneration and disease. Conditional deletion of Cripto in the myeloid lineage (CriptoMy-LOF ) perturbs MP plasticity in acutely injured muscle and in mouse models of Duchenne muscular dystrophy (mdx). Specifically, CriptoMy-LOF macrophages infiltrate the muscle, but fail to properly expand as anti-inflammatory CD206+ macrophages, which is due, at least in part, to aberrant activation of TGF?/Smad signaling. This reduction in macrophage plasticity disturbs vascular remodeling by increasing Endothelial-to-Mesenchymal Transition (EndMT), reduces muscle regenerative potential, and leads to an exacerbation of the dystrophic phenotype. Thus, in muscle-infiltrating macrophages, Cripto is required to promote the expansion of the CD206+ anti-inflammatory macrophage type and to restrict the EndMT process, providing a direct functional link between this macrophage population and endothelial cells.

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