IL-17A regulates the autophagic activity of osteoclast precursors through RANKL-JNK1 signaling during osteoclastogenesis in vitro.
Biochem Biophys Res Commun
; 497(3): 890-896, 2018 03 11.
Article
em En
| MEDLINE
| ID: mdl-29476739
ABSTRACT
Interleukin-17A(IL-17A), a proinflammatory cytokine, may have effects on osteoclastic resorption in inflammation-mediated bone loss, including postmenopausal osteoporosis. IL-17A could alter autophagic activity among other tissues and cells, thereby causing corresponding lesions. The aim of this study was to clarify how IL-17A influenced osteoclastogenesis by regulating autophagy. The present study showed that IL-17A could facilitate osteoclast precursors (OCPs) autophagy and osteoclastogenesis at a low concentration. Furthermore, suppression of autophagy with chloroquine (CQ) or 3-MA could significantly attenuate the enhanced osteoclastogenesis by a low level of IL-17A. It was also found that a low level of IL-17A couldn't up-regulate OCPs autophagy after removal of RANKL(Receptor Activator for Nuclear Factor-κB Ligand), and JNK(c-Jun N-terminal kinase) inhibitor only inhibited autophagy at a low level of IL-17A. These results suggest that a low concentration of IL-17A is likely to promote autophagic activity via activating RANKL-JNK pathway during osteoclastogenesis.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Osteoclastos
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Autofagia
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Transdução de Sinais
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Interleucina-17
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Proteína Quinase 8 Ativada por Mitógeno
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Ligante RANK
Limite:
Animals
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
China