MiR-149 suppresses the inflammatory response of chondrocytes in osteoarthritis by down-regulating the activation of TAK1/NF-κB.
Biomed Pharmacother
; 101: 763-768, 2018 May.
Article
em En
| MEDLINE
| ID: mdl-29524885
ABSTRACT
BACKGROUND:
Osteoarthritis (OA) is a degenerative joint disease that with the complication of disability, while inflammation is the important response of OA. MiR-149 was down-regulated in the OA tissues, while the potential mechanism of miR-149 in OA is unclear.METHODS:
A total of 20 OA patients and 20 healthy persons were enrolled in the present study. Real-time PCR was used to detect miR-149 and the mRNA expression of TAK1, western blot was used to detect the protein expression of TAK1. Luciferase reporter assay was performed to identify the targeting relationship between miR-149 and TAK1. Elisa assay was used to identify the level of several pro-inflammatory cytokines.RESULTS:
MiR-149 was down-regulated in both OA tissues and IL-1ß-induced chondrocytes, while the expression of TAK1 was opposite. TAK1 was the target gene miR-149 targets TAK1 to regulate its expression. Human normal chondrocytes subjected to IL-1ß significantly promoted the inflammatory response, and also accelerated the activation of NF-κB signaling pathway, while alternatively si-TAK1, miR-149 mimic or PDTC reversed the effects of IL-1ß. Cells transfected with miR-149 inhibitor promotes the level of inflammation cytokines, as well as the activation of NF-κB, while cells co-transfected with si-TAK1 and miR-149 inhibitor abolishes the effects of miR-149 inhibitor.CONCLUSION:
MiR-149 targets TAK1 to regulate the pathogenesis of OA, among which TAK1/NF-κB signaling acted as an important pathway in the inflammatory response that induced by IL-1ß.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Osteoartrite
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Regulação para Baixo
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NF-kappa B
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Mediadores da Inflamação
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MAP Quinase Quinase Quinases
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MicroRNAs
Tipo de estudo:
Prognostic_studies
Limite:
Adult
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Aged
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Aged80
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Biomed Pharmacother
Ano de publicação:
2018
Tipo de documento:
Article