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Nat Commun. 2017 May 18;8:15463. doi: 10.1038/ncomms15463.

Ccl2/Ccr2 signalling recruits a distinct fetal microchimeric population that rescues delayed maternal wound healing.

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INSERM UMRS_938, Saint-Antoine Research Center, 27, rue de Chaligny, Paris 75012, France.
UPMC Université Paris 6, 4, place Jussier, Paris 75005, France.
Université Paris 5 Descartes, 12, rue de l'Ecole de Médecine, Paris 75006, France.
Department of Dermatology, American University of Beirut, Riad EI Soph, Beinut 11072020, Lebanon.
Department of Dermatology, Hôpital Cochin, AP-HP, 89, rue d'Assas, Paris 75006, France.


Foetal microchimeric cells (FMCs) traffic into maternal circulation during pregnancy and persist for decades after delivery. Upon maternal injury, FMCs migrate to affected sites where they participate in tissue healing. However, the specific signals regulating the trafficking of FMCs to injury sites had to be identified. Here we report that, in mice, a subset of FMCs implicated in tissue repair displays CD11b+ CD34+ CD31+ phenotype and highly express C-C chemokine receptor 2 (Ccr2). The Ccr2 ligand chemokine ligand 2 (Ccl2) enhances the recruitment of FMCs to maternal wounds where these cells transdifferentiate into endothelial cells and stimulate angiogenesis through Cxcl1 secretion. Ccl2 administration improves delayed maternal wound healing in pregnant and postpartum mice but never in virgin ones. This role of Ccl2/Ccr2 signalling opens new strategies for tissue repair through natural stem cell therapy, a concept that can be later applied to other types of maternal diseases.

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