lncRNA PVT1 regulates chondrocyte proliferation and apoptosis through the glycolysis process mediated by miR-552-3p/PKM2 to promote osteoarthritis.

Osteoarthritis (OA) is a common degenerative joint disease, and cartilage dysfunction is the main cause of OA. Long non-coding RNAs (lncRNAs) have been reported to be involved in the development of OA, but the mechanism of action of lncRNA PVT1 (PVT1) in the progression of OA is still poorly understood. The purpose of this study was to explore the effect of lncRNA PVT1 on the progression of OA and the specific molecular mechanism. A rat OA model was constructed by surgery for medial meniscus instability of the right knee joint, and HC-a cells were treated with 10 μg/mL lipopolysaccharide (LPS) for 24 h to establish the OA cell model. The expression of related genes and proteins was detected by RT-qPCR and Western blot, and the damage of HC-a cells and articular cartilage tissue was evaluated by CCK-8, ELISA, flow cytometry, and HE staining. In this study, PVT1 was found to be upregulated in human or rat OA cartilage tissue, as well as in LPS-induced HC-a cells. Knockdown of PVT1 can alleviate the effect of LPS; promote the proliferation of HC-a cells; inhibit glycolysis, apoptosis, and the secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6; alleviate HC-a cell damage; and alleviate the development process of OA in vivo. Mechanistically, PVT1 upregulates the expression of PKM2 by inhibiting the expression of miR-552-3p, thereby promoting the glycolysis process and cell damage, and ultimately accelerating the occurrence and development of OA. Our study suggests that inhibition of PVT1 expression may be a new target for the treatment of OA.