miR-296-5p inhibits IL-1β-induced apoptosis and cartilage degradation in human chondrocytes by directly targeting TGF-β1/CTGF/p38MAPK pathway.

Osteoarthritis (OA) is characterized by apoptosis of chondrocytes and an imbalance of extracellular matrix (ECM) synthesis and catabolism. Emerging evidence has demonstrated that miRNAs are involved in OA pathologies, but the role of miR-296-5p in OA remains unclear. The present study proposes to reveal the functions and mechanisms of miR-296-5p in a cell model of OA. In this study, human chondrocytes were treated with 5 ml interleukin-1 beta (IL-1β) to induce apoptosis and cartilage degradation. Our results showed that miR-296-5p was downregulated in chondrocytes stimulated with IL-1β. Overexpressed miR-296-5p enhanced cell proliferation and inhibited apoptosis and matrix degrading enzyme expression in response to IL-1β stimulation, and knockdown of miR-296-5p showed the opposite effect. Further, we found that miR-296-5p directly targeted the 3'-untranslated region (3'-UTR) of TGF-β1 mRNA, and miR-296-5p inactivated the TGF-β1/CTGF/p38MAPK signaling pathway. Overexpression of TGF-β1 alleviated the inhibition of miR-296-5p on chondrocyte apoptosis and cartilage degradation. In conclusion, miR-296-5p inhibited the progression of OA through the CTGF/p38MAPK pathway by directly targeting TGF-β1.