Fig 2: miR-129-3p inhibits chondrocyte apoptosis through regulating CPEB1. CCK8 detected chondrocyte viability in each group (a); detection of cleaved caspase-3 expression by Western blot (b); apoptosis rate was examined by flow cytometry (c). ns, P > 0.05 compared to the OA group; #P < 0.05 compared to the OA + mimic NC group; $P < 0.05 compared to the OA + si-NC group; &P < 0.05 compared to the OA + miR-129-3p group. OA, osteoarthritis

Fig 3: Identification of primary chondrocytes and OA cellular model. Expression levels of miR-129-3p and CPEB1 in cartilage were determined by qRT-PCR analysis (a, b); correlation analysis of miR-129-3p with CPEB1 (c); the morphology of chondrocytes (× 100), results of toluidine blue staining (purple, × 100), immunofluorescent staining of type II collagen (green, × 200), DAPI staining (blue, × 200), and the merge graph (× 200) (d). After TNF-α treatment, flow cytometry and Western blot were applied to detect chondrocyte apoptosis and cleaved caspase-3 expression, respectively (e, f). **P < 0.01. OA, osteoarthritis

Fig 4: miR-129-3p negatively regulates CPEB1. The binding sites and mutant sites between CPEB1 and miR-129-3p (left), and interactions between miR-129-3p and CPEB1 were detected by dual luciferase reporter assay (right) (a); the regulation of miR-129-3p on the mRNA and protein expression levels of CPEB1 as measured by qRT-PCR (b) and Western blot (c). ns, P > 0.05, *P < 0.05 compared to the CPEB1 3′UTR WT group; #P < 0.05 compared to the mimic NC group; &P < 0.05 compared to inhibitor NC group