Hematopoietic and stromal DMP1-Cre labeled cells form a unique niche in the bone marrow.

Skeletogenesis and hematopoiesis are interdependent. Niches form between cells of both lineages where microenvironmental cues support specific lineage commitment. Because of the complex topography of bone marrow (BM), the identity and function of cells within specialized niches has not been fully elucidated.

Novel population of human monocyte and osteoclast progenitors from pluripotent stem cells and peripheral blood.

Osteoclasts are multinuclear cells of monocytic lineage, with the ability to resorb bone. Studies in mouse have identified bone marrow clonal progenitors able to generate mature osteoclast cells (OCs) in vitro and in vivo. These osteoclast progenitors (OCPs) can also generate macrophages and dendritic cells.

The NCI Center to Reduce Cancer Health Disparities: Moving Forward to Eliminate Cancer Health Disparities and Diversify the Cancer Biomedical Workforce.

The National Cancer Institute's (NCI) Center to Reduce Cancer Health Disparities (CRCHD) was established in 2001 with the purpose of confronting and eliminating cancer health disparities, while increasing workforce diversity in cancer research. Over the last two decades, CRCHD has generated a broad range of research, training, and community outreach activities to address these overarching goals through a variety of programs including the Continuing Umbrella of Research Experiences (CURE), Partnerships to Advance Cancer Health Equity (PACHE), Special Populations Networks (SPN), Community Networks Program (CNP), CNP Centers (CNPC), and Patient Navigation Research Program (PNRP). CRCHD, through its CURE and now its Intramural CURE (iCURE) programs, has been fully dedicated to training the next generation of competitive researchers from backgrounds typically underrepresented in the cancer and cancer health disparities research fields.

Osteoclasts Derive Predominantly from Bone Marrow-Resident CXCR1 Precursor Cells in Homeostasis, whereas Circulating CXCR1 Cells Contribute to Osteoclast Development during Fracture Repair.

Osteoclasts (OC) originate from either bone marrow (BM)-resident or circulating myeloid OC progenitors (OCP) expressing the receptor CXCR1. Multiple lines of evidence argue that OCP in homeostasis and inflammation differ. We investigated the relative contributions of BM-resident and circulating OCP to osteoclastogenesis during homeostasis and fracture repair.

Protease-Activated Receptor 1 Deletion Causes Enhanced Osteoclastogenesis in Response to Inflammatory Signals through a Notch2-Dependent Mechanism.

We found that protease-activated receptor 1 (PAR1) was transiently induced in cultured osteoclast precursor cells. Therefore, we examined the bone phenotype and response to resorptive stimuli of PAR1-deficient (knockout [KO]) mice. Bones and bone marrow-derived cells from PAR1 KO and wild-type (WT) mice were assessed using microcomputed tomography, histomorphometry, in vitro cultures, and RT-PCR.