Overexpressed miR-149 suppressed the IL-1β induced inflammation by decreasing the expressing TAK1, which mediated by NF-κB.

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.

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.

MiR-149 was down-regulated in both OA tissues and IL-1β-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-1β 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-1β. 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.

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-1β.