NFATc1 and NFATc3 is Involved in the Expression of Receptor Activator of NF-kappaB Ligand in Activated T Lymphocytes
International Journal of Oral Biology
;
: 37-42, 2013.
Artigo
em Coreano
| WPRIM
| ID: wpr-102154
ABSTRACT
Receptor activator of NF-kappaB ligand (RANKL) is an essential cytokine for osteoclast differentiation, activation and survival. T lymphocytes such as T17 cells, a subset of T helper cells that produce IL-17, play an important role in rheumatoid arthritic bone resorption by producing inflammatory cytokines and RANKL. It has not yet been clearly elucidated how T cell activation induces RANKL expression. T cell receptor activation induces the activation of nuclear factor of activated T cell (NFAT) and expression of its target genes. In this study, we examined the role of NFAT in T cell activation-induced RANKL expression. EL-4, a murine T lymphocytic cell line, was used. When T cell activation was induced by phorbol 12-myristate 13-acetate (PMA) and ionomycin, RANKL expression increased in a time-dependent manner. In the presence of cyclosporin, an inhibitor of NFAT activation, this PMA/ionomycin-induced RANKL expression was blocked. Overexpression of either NFATc1 or NFATc3 induced RANKL expression. Chromatin immunoprecipitation results demonstrated that PMA/ionomycin treatment induced the binding of NFATc1 and NFATc3 to the mouse RANKL gene promoter. These results suggest that NFATc1 and NFATc3 mediates T cell receptor activation-induced RANKL expression in T lymphocytes.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Osteoclastos
/
Reabsorção Óssea
/
Forbóis
/
Receptores de Antígenos de Linfócitos T
/
Linfócitos T
/
Ionomicina
/
Linhagem Celular
/
Citocinas
/
Ciclosporina
/
Linfócitos T Auxiliares-Indutores
Limite:
Animais
Idioma:
Coreano
Revista:
International Journal of Oral Biology
Ano de publicação:
2013
Tipo de documento:
Artigo
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