MicroRNAs have been extensively implicated in osteoarthritis (OA) progression. Our study aims to investigate the impact of miR-455-5p on OA progression and related molecular mechanisms. Cartilage tissues were collected from patients with OA and femoral neck fractures. An in vitro OA model was established by inducing injury in human chondrocytes (CHON-001) with interleukin (IL)-1 β. Cell viability and apoptosis were measured by cell counting kit-8 and flow cytometry assays, respectively. An enzyme-linked immunosorbent assay was performed to measure the concentrations of inflammation factors, and oxidative stress was evaluated by detecting superoxide dismutase activity and malondialdehyde levels. TargetScan was used to predict the binding sites between miR-455-5p and tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8), which were then confirmed by dual-luciferase reporter assays. Quantitative real-time polymerase chain reaction and western blot analysis were employed to measure the related molecular markers. Our initial observations showed that the expression of miR-455-5p was downregulated in OA cartilage and IL-1 β-treated CHON-001 cells compared to normal cartilage tissues and untreated cells. Overexpression of miR-455-5p significantly protected CHON-001 cells from IL-1 β-induced injury by recovering cell viability, and inhibiting inflammation, apoptosis, and oxidative stress. TNFAIP8 was targeted by miR-455-5p and negatively regulated by miR-455-5p. TNFAIP8 knockdown imitated, while overexpression reversed the effects mediated by miR-455-5p in IL-1 β-induced chondrocyte injury, as further confirmed by the protein levels of iNOS, cleaved caspase-3, NQO1, Col2a1, and MMP13. Collectively, these results suggest that miR-455-5p may serve as a new therapeutic target for OA by targeting TNFAIP8 to alleviate IL-1 β-induced chondrocyte injury.
Keywords: CHON-001; interleukin 1 β; miR-455-5p; osteoarthritis; tumor necrosis factor AIP8.
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