Serum amyloid A inhibits RANKL-induced osteoclast formation
Experimental & Molecular Medicine
;
: e194-2015.
Artigo
em Inglês
| 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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Osteoclastos
/
Proteína Amiloide A Sérica
/
Diferenciação Celular
/
Linhagem Celular
/
Trifosfato de Adenosina
/
Receptor de Fator Estimulador de Colônias de Macrófagos
/
Regulação da Expressão Gênica no Desenvolvimento
/
Receptores de Formil Peptídeo
/
Receptor 2 Toll-Like
/
Receptor 4 Toll-Like
Limite:
Animais
/
Humanos
Idioma:
Inglês
Revista:
Experimental & Molecular Medicine
Ano de publicação:
2015
Tipo de documento:
Artigo
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