Rac signaling in osteoblastic cells is required for normal bone development but is dispensable for hematopoietic development.

摘要: Hematopoietic stem cells (HSCs) interact with osteoblastic, stromal, and vascular components of the BM hematopoietic microenvironment (HM) that are required for maintenance long-term self-renewal in vivo. Osteoblasts have been reported to be a critical cell type making up HSC niche Rac1 GTPase has implicated adhesion, spreading, differentiation osteoblast lines is engraftment retention. Recent data suggest differential role GTPases endosteal/osteoblastic versus perivascular function. However, whether Rac signaling pathways also necessary cell-extrinsic control function within HM not examined. In present study, genetic inducible models deletion were used demonstrate depletion causes impaired proliferation induction apoptosis OP9 line primary stromal cells. Deletion proteins caused reduced trabecular cortical long bone growth Surprisingly, hematopoiesis vivo was preserved despite these substantial changes. These implications therapeutic strategies target mobilization treatment leukemia provide clarification our evolving concepts HSC-HM interactions.