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Serum amyloid A inhibits RANKL-induced osteoclast formation
Experimental & Molecular Medicine ; : e194-2015.
Article in English | WPRIM | ID: wpr-55050
ABSTRACT
When mouse bone marrow-derived macrophages were stimulated with serum amyloid A (SAA), which is a major acute-phase protein, there was strong inhibition of osteoclast formation induced by the receptor activator of nuclear factor kappaB ligand. SAA not only markedly blocked the expression of several osteoclast-associated genes (TNF receptor-associated factor 6 and osteoclast-associated receptor) but also strongly induced the expression of negative regulators (MafB and interferon regulatory factor 8). Moreover, SAA decreased c-fms expression on the cell surface via shedding of the c-fms extracellular domain. SAA also restrained the fusion of osteoclast precursors by blocking intracellular ATP release. This inhibitory response of SAA is not mediated by the well-known SAA receptors (formyl peptide receptor 2, Toll-like receptor 2 (TLR2) or TLR4). These findings provide insight into a novel inhibitory role of SAA in osteoclastogenesis and suggest that SAA is an important endogenous modulator that regulates bone homeostasis.
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Osteoclasts / Serum Amyloid A Protein / Cell Differentiation / Cell Line / Adenosine Triphosphate / Receptor, Macrophage Colony-Stimulating Factor / Gene Expression Regulation, Developmental / Receptors, Formyl Peptide / Toll-Like Receptor 2 / Toll-Like Receptor 4 Limits: Animals / Humans Language: English Journal: Experimental & Molecular Medicine Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Osteoclasts / Serum Amyloid A Protein / Cell Differentiation / Cell Line / Adenosine Triphosphate / Receptor, Macrophage Colony-Stimulating Factor / Gene Expression Regulation, Developmental / Receptors, Formyl Peptide / Toll-Like Receptor 2 / Toll-Like Receptor 4 Limits: Animals / Humans Language: English Journal: Experimental & Molecular Medicine Year: 2015 Type: Article