NLRC5 promotes cell proliferation via regulating the NF-κB signaling pathway in Rheumatoid arthritis.
Mol Immunol
; 91: 24-34, 2017 11.
Article
en En
| MEDLINE
| ID: mdl-28865311
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease and the pathogenesis remains unclear. Previous studies suggested that fibroblast-like synoviocytes (FLSs) play an important role in RA pathogenesis, including the injury of cartilage, the hyperplasia of the synovium and the release of inflammatory cytokines. We used complete Freund's adjuvant (CFA) induced rats as animal models for studying the RA pathogenesis. NLRC5 as the largest member of the NLR family has been reported to play a critical role in regulating immune responses. Increasing evidence suggests that NLRC5 is an pivotal negative modulator of inflammatory pathways. We investigated the mechanisms and signaling pathways of NLRC5 in RA progression. Significantly increased expression of NLRC5 was found in AA rats synovial tissues and cells. And high expression of inflammatory cytokine and cell proliferation of FLSs accompanied with NLRC5 overexpression, but inhibited in cells with NLRC5 silencing treatment. Interestingly, we found that overexpression of NLRC5 also coordinated the activation of NF-κB signaling pathway. These results suggested that NLRC5 promotes RA progression via the NF-κB signaling pathway potentially.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Artritis Reumatoide
/
Transducción de Señal
/
Regulación de la Expresión Génica
/
FN-kappa B
/
Péptidos y Proteínas de Señalización Intracelular
/
Proliferación Celular
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Mol Immunol
Año:
2017
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido