Background/Aims: MicroRNAs (miRNAs) are involved in the pathogenesis of OA. This study aimed to investigate the potential function of miR-122 in the development of OA and its potential molecular mechanisms. Methods: The expression of miR-122 , SIRT1, collagen II, aggrecan, MMP13 and ADAMTS4 in OA cartilage was detected by RT-qPCR. Target gene prediction and screening, luciferase reporter assay were used to verify downstream target genes of miR-122. Results: Compared with osteonecrosis, the expression of miR-122 was significantly increased in OA cartilage, while the expression of SIRT1 was significantly decreased. Overexpression of microRNA-122 increased the expression of ECM catabolic factors, for example disintegrins, matrix metalloproteinases and metalloproteinases with platelet reaction protein motifs, and inhibited the expression of synthetic metabolic genes such as collagen II and aggregating proteoglycan. Inhibition of miR-122 expression had the opposite effect. Furthermore, SIRT1 was identified as a direct target of miR-122. SIRT1 was significantly inhibited by miR-122 overexpression. Knockdown of SIRT1 reversed the degradation of chondrocyte ECM by miR-122 inhibitors. Conclusion: The miR-122 / SIRT1 axis can regulate the degradation of extracellular matrix in OA, thus providing new insights for the treatment of OA.

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