Erythro-myeloid progenitor origin of Hofbauer cells in the early mouse placenta.

Autor:	Freyer L; Institut Pasteur, Unit for Macrophages and Endothelial Cells, Developmental and Stem Cell Biology Department, UMR3738 CNRS, 75015 Paris, France., Lallemand Y; Institut Pasteur, Unit for Macrophages and Endothelial Cells, Developmental and Stem Cell Biology Department, UMR3738 CNRS, 75015 Paris, France., Dardenne P; Institut Pasteur, Unit for Macrophages and Endothelial Cells, Developmental and Stem Cell Biology Department, UMR3738 CNRS, 75015 Paris, France., Sommer A; Institut Pasteur, Unit for Macrophages and Endothelial Cells, Developmental and Stem Cell Biology Department, UMR3738 CNRS, 75015 Paris, France.; Sorbonne Université, Collège Doctoral, F-75005 Paris, France., Biton A; Bioinformatics and Biostatistics Hub, Institut Pasteur, 75015 Paris, France., Gomez Perdiguero E; Institut Pasteur, Unit for Macrophages and Endothelial Cells, Developmental and Stem Cell Biology Department, UMR3738 CNRS, 75015 Paris, France.
Jazyk:	angličtina
Zdroj:	Development (Cambridge, England) [Development] 2022 Apr 15; Vol. 149 (8). Date of Electronic Publication: 2022 Apr 22.
DOI:	10.1242/dev.200104
Abstrakt:	Hofbauer cells (HBCs) are tissue macrophages of the placenta thought to be important for fetoplacental vascular development and innate immune protection. The developmental origins of HBCs remain unresolved and could implicate functional diversity of HBCs in placenta development and disease. In this study, we used flow cytometry and paternally inherited reporters to phenotype placenta macrophages and to identify fetal-derived HBCs and placenta-associated maternal macrophages in the mouse. In vivo pulse-labeling traced the ontogeny of HBCs from yolk sac-derived erythro-myeloid progenitors, with a minor contribution from fetal hematopoietic stem cells later on. Single-cell RNA-sequencing revealed transcriptional similarities between placenta macrophages and erythro-myeloid progenitor-derived fetal liver macrophages and microglia. As with other fetal tissue macrophages, HBCs were dependent on the transcription factor Pu.1, the loss-of-function of which in embryos disrupted fetoplacental labyrinth morphology, supporting a role for HBC in labyrinth angiogenesis and/or remodeling. HBC were also sensitive to Pu.1 (Spi1) haploinsufficiency, which caused an initial deficiency in the numbers of macrophages in the early mouse placenta. These results provide groundwork for future investigation into the relationship between HBC ontogeny and function in placenta pathophysiology. Competing Interests: Competing interests The authors declare no competing or financial interests. (© 2022. Published by The Company of Biologists Ltd.)
Databáze:	MEDLINE
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