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Dev Cell. 2012 Mar 13;22(3):651-9. doi: 10.1016/j.devcel.2011.12.022. Epub 2012 Mar 1.

Trophoblasts regulate the placental hematopoietic niche through PDGF-B signaling.

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  • 1Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.

Abstract

The placenta is a hematopoietic organ that supports hematopoietic stem/progenitor cell (HSPC) generation and expansion without promoting differentiation. We identified PDGF-B signaling in trophoblasts as a key component of the unique placental hematopoietic microenvironment that protects HSPCs from premature differentiation. Loss of PDGF-B or its receptor, PDGFRβ, induced definitive erythropoiesis in placental labyrinth vasculature. This was evidenced by accumulation of CFU-Es and actively proliferating definitive erythroblasts that clustered around central macrophages, highly reminiscent of erythropoiesis in the fetal liver. Ectopic erythropoiesis was not due to a requirement of PDGF-B signaling in hematopoietic cells but rather in placental trophoblasts, which upregulated Epo in the absence of PDGF-B signaling. Furthermore, overexpression of hEPO specifically in the trophoblasts in vivo was sufficient to convert the placenta into an erythropoietic organ. These data provide genetic evidence of a signaling pathway that is required to restrict erythroid differentiation to specific anatomical niches during development.

Copyright © 2012 Elsevier Inc. All rights reserved.

PMID:
22387002
[PubMed - indexed for MEDLINE]
PMCID:
PMC3395466
Free PMC Article

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