Journal
DEVELOPMENTAL CELL
Volume 22, Issue 3, Pages 651-659Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2011.12.022
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Funding
- NIH [RO1 HL097766-01, RO1 HL074257]
- Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA
- California Institute for Regenerative Medicine [T1-00005, TG2-01169]
- Jonsson Comprehensive Cancer Center Foundation at UCLA
- Howard Hughes Undergraduate Research Program
- Japan Society for the Promotion of Science
- Ruth L. Kirschstein National Research Service Award [GM007185]
- NIH/NHLBI [T32 HL69766]
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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, PDGFR beta, 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.
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