LINC00707 knockdown inhibits IL-1β-induced apoptosis and extracellular matrix degradation of osteoarthritis chondrocytes by the miR-330-5p/FSHR axis.

BACKGROUND

Osteoarthritis (OA) is a severe disabling condition that causes major health problems. The roles of long non-coding RNAs (lncRNAs) in regulating OA progression have been increasingly researched. Based on previously published microarray analysis, LINC00707 is upregulated in OA. This research was done to uncover the function of LINC00707 in IL-1β-induced chondrocyte injury and its possible mechanisms.

METHODS

LINC00707, miR-330-5p, and follicle-stimulating hormone receptor (FSHR) expression in OA cartilage tissues were assessed by RT-qPCR. Primary chondrocytes were isolated from OA tissues and treated with IL-1β to establish an OA model. Under the indicated treatment, chondrocyte apoptosis, senescence, ECM degradation, and inflammation were determined using flow cytometry, TUNEL, SA-β-Gal staining, and ELISA experiments, respectively. Interactions between gene were evaluated using Ago2 RIP and luciferase reporter assays.

RESULTS

LINC00707 and FSHR were elevated, and miR-330-5p was reduced in cartilage tissues of OA patients and in IL-1β-treated primary chondrocytes. Silencing LINC00707 hampered chondrocytes apoptosis, senescence, ECM degradation, and inflammation. LINC00707 acted as a ceRNA to regulate FSHR through controlling miR-330-5p availability. Additionally, both miR-330-5p depletion and FSHR overexpression diminished the effects of silencing LINC00707 in OA progression.

CONCLUSIONS

Silencing LINC00707 mitigates chondrocyte injury in osteoarthritis sponging miR-330-5p and inhibiting FSHR.