LncRNA TUG1 promotes osteoarthritis-induced degradation of chondrocyte extracellular matrix via miR-195/MMP-13 axis.

Abstract

Osteoarthritis is a degenerative disease characterized by articular cartilage degradation. Long non-coding ribonucleic acid (lncRNA) plays important roles in a series of biological processes, but its role in osteoarthritis is still not quite clear. This study aims to investigate the regulatory role of taurine upregulated gene 1 (TUG1) in osteoarthritis. The expression level of lncRNA-TUG1 in cartilages of patients with osteoarthritis and those of normal people was compared using Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Primary chondrocytes were induced by interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α), followed by expression detection of lncRNA-TUG1, microRNA-195 (miR-195), and matrix metalloproteinase-13 (MMP-13). In addition, in vitro regulatory roles of lncRNA-TUG1 and miR-195 in osteoarthritis were verified by transfection of lncRNA-TUG1 and miR-195 plasmids. The dimethylmethylene blue (DMMB) assay was performed to analyze the secretion and formation of soluble sulfated glycosaminoglycan (sGAG). The expression levels of lncRNA-TUG1 and MMP-13 in cartilages of patients with osteoarthritis were higher than those in cartilages of normal people, while the level of miR-195 decreased in cartilages of patients with osteoarthritis. After chondrocytes were induced by IL-1β and TNF-α, the expression of lncRNA-TUG1 increased. Overexpression of lncRNA-TUG1 decreased the expressions of miR-195, collagen, and aggrecan, but increased the expression of MMP-13. LncRNA-TUG1 knockdown obtained the opposite results. LncRNA-TUG1 regulates the degradation of extracellular matrix in osteoarthritis via lncRNA-TUG1/miR-195/MMP-13 axis.