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

Nature Communications
Mathieu CastelaS Aractingi

Abstract

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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Citations

Jan 30, 2018·Cellular & Molecular Immunology·Teizo Yoshimura
Sep 30, 2020·Annals of the New York Academy of Sciences·Sangeetha Vadakke-Madathil, Hina W Chaudhry
Aug 23, 2019·Fetal and Pediatric Pathology·M Sinan BeksacMeral Beksac
Oct 14, 2017·Briefings in Functional Genomics·Anders StåhlbergThomas Kroneis
Mar 2, 2021·Frontiers in Immunology·Lisa KornstädtKlaus Scholich
Jul 1, 2021·American Journal of Reproductive Immunology : AJRI·Chun-Yan WeiDa-Jin Li
Aug 13, 2021·Stem Cell Reviews and Reports·Margit RosnerMarkus Hengstschläger

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Methods Mentioned

BETA
PCR
FACS
transgenic
Hi-Seq
biopsy
electrophoresis

Software Mentioned

ImageJ
Graphpad Prism
FlowJo

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