Knockdown of LINC01385 inhibits osteoarthritis progression by modulating the microRNA-140-3p/TLR4 axis.

Long non-coding (lnc) RNAs have been associated with osteoarthritis (OA) progression. The aim of the present study was to investigate the regulatory mechanism of lncRNA LINC01385 in OA . The mRNA expression level of LINC01385, microRNA(miR)-140-3p, and Toll-like receptor 4 (TLR4) was detected using reverse transcription-quantitative PCR, while ELISA was used to determine the concentration of different inflammatory factors [tumor necrosis factor-α (TNF-α), IL-6, and prostaglandin E (PGE)]. The viability of human articular chondrocytes (HC-a) was measured using a MTT assay and western blot analysis was performed to quantify the protein expression level of TLR4. The associations between miR-140-3p and LINC01385/TLR4 were confirmed using a dual-luciferase reporter assay. LINC01385 mRNA expression level was increased in OA tissues and IL-1β-induced HC-a. LINC01385 knockdown and miR-140-3p mimics reduced the concentration of inflammatory factors in IL-1β-induced HC-a and promoted cell survival. In addition, it was confirmed that LINC01385 targeted miR-140-3p, while was a target gene of miR-140-3p. Negative correlations between LINC01385 and miR-140-3p, and between miR-140-3p and TLR4 were observed in OA tissues. Low mRNA expression level of miR-140-3p and high protein expression level of TLR4 reversed the inhibitory effect of LINC01385 knockdown on the inflammatory responses of IL-1β-induced HC-a and exhibited a stimulating effect on cell viability. LINC01385 knockdown reduced the progression of OA by modulating the miR-140-3p/TLR4 axis ; thus, LINC01385 may be a therapeutic target for OA.