| First Author | Raman R | Year | 2013 |
| Journal | Leukemia | Volume | 27 |
| Issue | 11 | Pages | 2209-19 |
| PubMed ID | 23563238 | Mgi Jnum | J:202796 |
| Mgi Id | MGI:5521456 | Doi | 10.1038/leu.2013.103 |
| Citation | Raman R, et al. (2013) p190-B RhoGAP regulates the functional composition of the mesenchymal microenvironment. Leukemia 27(11):2209-19 |
| abstractText | Hematopoiesis is regulated by components of the microenvironment, so-called niche. Here, we show that p190-B GTPase-activating protein (p190-B) deletion in mice causes hematopoietic failure during ontogeny, in p190-B(-/-) fetal liver and bones, and in p190-B(+/-) adult bones and spleen. These defects are non-cell autonomous, as we previously showed that transplantation of p190-B(-/-) hematopoietic cells into wild-type (WT) hosts leads to normal hematopoiesis. Coculture of mesenchymal stem (MSC)/progenitor cells and wild-type bone marrow (BM) cells reveals that p190-B(-/-) MSCs are dysfunctional in supporting hematopoiesis owing to impaired Wnt signaling. Furthermore, p190-B loss causes alteration in BM niche composition, including abnormal colony-forming unit (CFU)-fibroblast, CFU-adipocyte and CFU-osteoblast numbers. This is due to altered MSC lineage fate specification to osteoblast and adipocyte lineages. Thus, p190-B organizes a functional mesenchymal/microenvironment for normal hematopoiesis during development. |
