| First Author | Chhabra A | Year | 2012 |
| Journal | Dev Cell | Volume | 22 |
| Issue | 3 | Pages | 651-9 |
| PubMed ID | 22387002 | Mgi Jnum | J:182738 |
| Mgi Id | MGI:5316528 | Doi | 10.1016/j.devcel.2011.12.022 |
| Citation | Chhabra A, et al. (2012) Trophoblasts regulate the placental hematopoietic niche through PDGF-B signaling. Dev Cell 22(3):651-9 |
| abstractText | 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, PDGFRbeta, 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. |
