Objective To investigate the effects of lncRNA LINC00470/PI3K pathway activation on the autophagy of bone and joint in knee osteoarthritis(OA) model.

Methods Human articular cartilage samples, OA model rats and IL-1β-treated C28/I2 cells were used in this study. The expression changes of genes and proteins were assessed by real-time quantitative PCR(RT-qPCR) and Western blotting. The cell viability, apoptosis and autophagy were assessed by CCK-8, flow cytometry, immunofluorescence and Western blotting analysis, respectively. Masson staining and TUNEL staining were performed in vivo to evaluate cartilage tissue Mankin score and apoptosis.

Results The LINC00470 was upregulated in OA patients and IL-1β-induced chondrocytes. IL-1β treatment decreased C28/I2 cell viability, increased apoptosis and inhibited autophagy, which were largely reversed by LINC00470 knockdown. The LINC00470 knockdown in C28/I2 cells abolished IL-1β-induced activation of PI3K/AKT/mTOR signaling. In a rat model of OA, LINC00470 knockdown decreased Mankin score, reduced apoptosis, promoted autophagy, and inhibited activation of PI3K/AKT/mTOR signaling.

Conclusions LINC00470 promotes autophagy in OA, which may depend on the PI3K/AKT/mTOR signaling pathway.