Expression of miR-671 was reported to be downregulated in articular cartilage of patients with OA compared to healthy individuals, indicating it may serve as potential biomarker for OA. However, the mechanism by which miR-671 regulates the progression of OA remains unclear. Here, we aimed to investigate the role of miR-671 in cartilage from patients with OA.
The expression of miR-671 and inflammation mediators in cartilage from patients with OA was analyzed by RT-PCR. In vitro, chondrocytes CHON-001 were stimulated with IL-1β for 24 h for OA model establishment. Protein expression of MMP-13, aggrecan, and collagen II was measured by western blot. In vivo, the severity of OA in mice was determined by histological analysis.
We found that the level of miR-671 was downregulated in OA tissues, plasma and IL-1β treated CHON-001 cells, compared with control. MiR-671 mimics ameliorated IL-1β-induced proliferation inhibition and apoptosis stimulation, as well as decreased protein levels of collagen II and aggrecan in CHON-001 cells. In vivo study showed miR-671 mimics alleviated the progression of OA in mice.
These results indicated miR-671 play an important role during the pathogenesis of OA. Therefore, miR-671 may serve as a potential therapeutic target for the treatment of OA.