CircTMBIM6 promotes osteoarthritis-induced chondrocyte extracellular matrix degradation via miR-27a/MMP13 axis

摘要

OBJECTIVE: Osteoarthritis is a degenerative disease characterized by degeneration of articular cartilage, but the current mechanism is unclear. Circular RNA (circRNA) plays a significant role in a series of biological processes related to osteoarthritis, but its mechanism remains unclear. The purpose of this study was to investigate the role of the circTMBIM6/miR-27a/MMP13 axis in osteoarthritis. PATIENTS AND METHODS: The expression levels of circTMBIM6, miR-27a and MMP13 in cartilage of osteoarthritis patients and normal human cartilage were detected by reverse transcription polymerase chain reaction (RT-PCR). Osteoarthritis cell model was induced by IL-1β and TNF-α, and the expression changes of circTMBIM6, miR-27a and MMP13 in the in vitro model were detected. In addition, the in vitro regulation of circTMBIM6 and miR-27a in osteoarthritis was verified by transfection of circTMBIM6 and miR-27a plasmids, and the regulation of miR-27a on MMP13 was also verified. The dimethylmethylene blue (DMMB) method was used to analyze the secretion and formation of soluble glycosaminoglycan sulfate (sGAG), and the effects of circTMBIM6 and miR-27a chondrocytes were evaluated. RESULTS: The expression levels of circTMBIM6 and MMP13 in cartilage tissue of patients with osteoarthritis were higher than that of normal group, while the expression level of miR-195 in cartilage tissue of patients with osteoarthritis was lower. After IL-1β and TNF-α treatment, the expression of circTMBIM6 and MMP13 in chondrocytes increased, while the expression of miR-27a decreased. CircTMBIM6 overexpression reduced miR-27a expression but increased MMP13 expression. The circTMBIM6 gene knockout showed the opposite effect. CONCLUSIONS: CircTMBIM6 promotes osteoarthritis-induced chondrocyte extracellular matrix degradation via miR-27a/MMP13 axis.