Long Non-Coding RNA Plasmacytomavariant Translocation1 as ceRNA Adsorbs miR-195 to Relieve Osteoarthritis Symptoms

Abstract

This study aimed to investigate the role of the long non-coding RNA plasmacytomavariant translocation1 (LncRNA PVT1) in the development of osteoarthritis (OA). The study used mice and performed DMM surgery to establish an OA model. PVT1 and miR-195 agomir were inhibited in the knee joints, and cartilage tissue specimens were collected for gene expression analysis, apoptotic protein detection, histopathological observation, and Mankin’s score evaluation. Enzymelinked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in peripheral blood and cartilage tissues. Terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining was used to detect cartilage cell apoptosis. The results indicated that the OA group had higher plasmacytomavariant translocation1 (PVT1) expression and lower miR-195 expression than the sham-operated group. PVT1 was found to act as a molecular sponge for miR-195 through a dual-luciferase reporter assay. Knocking down PVT1 or upregulating miR-195 significantly attenuated inflammation and apoptosis in the bone joints of OA mice. This study provides new insights into the mechanism of OA progression and suggests that regulating the PVT1-miR-195 axis may be beneficial for improving the inflammatory microenvironment of cartilage tissue and apoptosis.