MicroRNA-613 alleviates IL-1β-induced injury in chondrogenic CHON-001 cells by targeting fibronectin 1.

BACKGROUND Osteoarthritis (OA) is an aging-related chronic degenerative joint disease. A number of miRNAs have been found to be involved in the development of OA, but the role of miR-613 in OA remains unclear. Thus, this study aimed to investigate the role of miR-613 during the progression of OA. METHODS CHON-001 cells were transfected with miR-613 agonist for 48 h, and then exposed to 10 ng/mL IL-1β for 24 h. Cell viability, cell proliferation and cell apoptosis in CHON-001 cells were assessed by CCK-8, immunofluorescence, and flow cytometry assays, respectively. In addition, the dual luciferase reporter system assay was used to determine the interaction of miR-613 and fibronectin 1 in CHON-001 cells. RESULTS The level of miR-613 was significantly decreased in IL-1β-treated CHON-001 cells. Overexpression of miR-613 markedly inhibited IL-1β-induced apoptosis in CHON-001 cells. In addition, upregulation of miR-613 obviously alleviated IL-1β-induced inflammatory response and cartilage matrix degradation in CHON-001 cells. Meanwhile, fibronectin 1 was identified as a direct binding target of miR-613 in CHON-001 cells. Overexpression of miR-613 alleviated IL-1β-induced injury in CHON-001 cells via downregulating the expression of fibronectin 1. Furthermore, overexpression of miR-613 alleviated cartilage degradation, and reduced OARSI scores and subchondral bone thickness in a mouse model of OA. CONCLUSION Our data indicated that overexpression of miR-613 could inhibit IL-1β-induced injury in CHON-001 cells via decreasing the level fibronectin 1 in vitro, and alleviate the symptoms of OA in vivo. Therefore, miR-613 might be a potential therapeutic option for the treatment of OA.