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Philip Osdoby

Researcher at Washington University in St. Louis

Publications -  55
Citations -  3721

Philip Osdoby is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Osteoclast & Bone resorption. The author has an hindex of 30, co-authored 55 publications receiving 3571 citations. Previous affiliations of Philip Osdoby include Saint Louis University & University of Washington.

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Receptor Activator of NF-κB and Osteoprotegerin Expression by Human Microvascular Endothelial Cells, Regulation by Inflammatory Cytokines, and Role in Human Osteoclastogenesis *

TL;DR: It is shown for the first time that human microvascular endothelial cells (HMVEC) express transcripts for both RankL and OPG; inflammatory cytokines tumor necrosis factor-α and interleukin-1α elevate RANKL andOPG expression 5–40-fold in HMVEC; and cytokine-activated VEC may contribute to inflammatory-mediated bone loss via regulated production of RANKl and O PG.
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Potentiation of osteoclast bone-resorption activity by inhibition of nitric oxide synthase

TL;DR: Findings suggest that endogenous NO production in osteoclast cultures may regulate resorption activity, and the modulation of NOS and NO levels by cells within the bone microenvironment may be a sensitive mechanism for local control of osteoporosis.
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Stromal cell-derived factor-1 (SDF-1) recruits osteoclast precursors by inducing chemotaxis, matrix metalloproteinase-9 (MMP-9) activity, and collagen transmigration.

TL;DR: In this paper, SDF-1 and RANKL were analyzed during osteoclast (OC) formation induced by RANKl in murine RAW 264.7 cells, and the results showed that SDF1 increased MMP-9, a matrix-degrading enzyme essential for bone marrow cavities, and increased transcollagen migration of RAW cells in a MMPdependent manner.
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Stromal cell-derived factor-1 binding to its chemokine receptor CXCR4 on precursor cells promotes the chemotactic recruitment, development and survival of human osteoclasts

TL;DR: It is demonstrated for the first time that SDF-1 chemoattracts circulating human Oc precursors capable of developing into bone-resorptive Oc, and that it can stimulate MN cell fusion and TRAP activity, mimic M-CSF + RANKL in early osteoclastogenic effects, substitute for M- CSF - RANKl in maintaining the survival of mature human OC, and suppress Oc expression of Bim protein.
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CCR1 chemokines promote the chemotactic recruitment, RANKL development, and motility of osteoclasts and are induced by inflammatory cytokines in osteoblasts.

TL;DR: Cytokines induced OB release of such chemokines, which may therefore significantly contribute to inflammatory bone loss.