Abstract
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, since we previously showed that transplantation of p190-B−/− hematopoietic cells into wild-type hosts leads to normal hematopoiesis. Coculture of mesenchymal stem/progenitor cells (MSC) and wild-type bone marrow cells reveals that p190-B−/− MSCs are dysfunctional in supporting hematopoiesis due to impaired Wnt signaling. Furthermore, p190-B loss causes alteration in bone marrow niche composition, including abnormal 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.
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