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Session 7, Abstract 38


Asmaa Mohamed* and Gabriela G. Loots (Jennifer O. Manilay), Molecular and Cellular Biology Unit, School of Natural Sciences, University of California, Merced 

The role of sclerostin (SOST) and the molecular mechanisms that mediate the crosstalk between HSCs and the different bone marrow niche cells are incompletely understood. Previous data from our laboratory showed that SOST knockout (KO) mice had a higher bone mass, smaller bone marrow cavity and fewer CD45+ hematopoietic cells in the bone marrow compared to wild type controls. Paradoxically, our preliminary data indicate that hematopoietic stem cells (HSCs) in SOST-KO bones may be more proliferative than controls. Our goal is to understand the molecular mechanisms that regulate HSC proliferation in SOST-KO mice. We hypothesize that specific bone “niche cells” control HSC proliferation. To test this hypothesis, we need to optimize our bone niche cell isolation protocol in order to collect endothelial cells, osteoblasts, and mesenchymal stem cells from whole bones. Optimization of this protocol will allow us to then perform functional HSC-niche cell co-culture assays, as well as analysis of gene expression in the specific bone niche cells. The results of these studies could identify the specific niche cell in the bone that induces HSC proliferation, which could have applications for hematological diseases and immunity.