Circ_0114876 promoted IL-1β-induced chondrocyte injury by targeting miR-671/TRAF2 axis

• Published in: Biotechnology letters 2021-04, Vol.43 (4), p.791-802
• Main Authors: Wang, Qiushi, Luo, Simin, Yang, Jie, Li, Jieruo, Huan, Songwei, She, Guorong, Zha, Zhengang
• Format: Article
• Language: English
• Subjects: Apoptosis; Applied Microbiology; Biochemistry; Biomedical and Life Sciences; Biomedical materials; Biotechnology; Cell viability; Chondrocytes; IL-1β; Inflammation; Joint diseases; Life Sciences; Microbiology; Original Research Paper; Osteoarthritis; Regulatory mechanisms (biology); TRAF2 protein
• ISSN: 0141-5492; 1573-6776
• DOI: 10.1007/s10529-020-03070-1

Osteoarthritis (OA) is a chronic joint disease, which occurs in the elderly. The regulatory mechanisms of circRNAs were involved in the occurrence and development of various diseases. However, the potential regulatory network of circRNA in OA remains further research and clarification. The expression of circ_0114876 was increased in OA tissues and inhibition of circ_0114876 could induce cell viability and suppress inflammation as well as inhibit cell apoptosis in IL-1β induced CHON-001 cells. Circ_0114876 regulated TRAF2 expression via sponging miR-671 in CHON-001 cells. Down-regulated miR-671 expression could reverse the effects of low circ_0114876 expression on cell progression and inflammation in IL-1β induced CHON-001 cells. Overexpression of TRAF2 could weaken the promotion effects of high miR-671 expression on cell progression and inflammation in IL-1β induced CHON-001 cells. Circ_0114876 targeted miR-671 to regulate cell progression and inflammation via modulating TRAF2 expression in IL-1β induced CHON-001 cells, and played an important regulatory mechanism in IL-1β-induced chondrocyte injury, providing a novel diagnostics and therapeutics in OA.