MicroRNA‑671‑3p regulates the development of knee osteoarthritis by targeting TRAF3 in chondrocytes.

Abstract

Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation and joint inflammation. A previous study showed that microRNA (miR)‑671‑3p is involved in the development of OA, however, its function and molecular target in chondrocytes during the pathogenesis of OA remain to be fully elucidated. In the present study, miR‑671‑3p was significantly downregulated in knee OA cartilage tissues compared with normal cartilage tissues. The expression levels of pro‑inflammatory cytokines, including interleukin (IL)‑1β, IL‑6, IL‑8 and tumor necrosis factor (TNF)‑α, in the knee OA cartilage tissues were significantly higher than those in the normal cartilage tissues. Through gain‑of‑function and loss‑of‑function experiments, miR‑671‑3p was shown to significantly affect matrix synthesis gene expression, cell proliferation, apoptosis and inflammation in chondrocytes from patients with OA. Subsequent bioinformatics analysis identified potential target sites of the miR‑671‑3p located in the 3'untranslated region of TNF receptor‑associated factor (TRAF3). The results of a dual‑luciferase reporter assay showed that TRAF3 is a target gene of miR‑671‑3p. Western blot analysis demonstrated that miR‑671‑3p inhibited the gene expression of TRAF3. Furthermore, the restoration of TRAF3 markedly abrogated the effect of miR‑671‑3p. Taken together, the present study suggests that miR‑671‑3p may be important in the pathogenesis of OA through targeting TRAF3 and regulating chondrocyte apoptosis and inflammation, which may be a potential molecular target for OA treatment.