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.
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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