Serum amyloid A inhibits RANKL-induced osteoclast formation
Experimental & Molecular Medicine
;
: e194-2015.
Artículo
en Inglés
| 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:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Osteoclastos
/
Proteína Amiloide A Sérica
/
Diferenciación Celular
/
Línea Celular
/
Adenosina Trifosfato
/
Receptor de Factor Estimulante de Colonias de Macrófagos
/
Regulación del Desarrollo de la Expresión Génica
/
Receptores de Formil Péptido
/
Receptor Toll-Like 2
/
Receptor Toll-Like 4
Límite:
Animales
/
Humanos
Idioma:
Inglés
Revista:
Experimental & Molecular Medicine
Año:
2015
Tipo del documento:
Artículo
Similares
MEDLINE
...
LILACS
LIS