Qiaojie Chen1, Shaokun Wu1, Yaojun Wu1, Liang Chen1, Qingjiang Pang2. 1. Department of Orthopaedics Surgery, Ningbo No. 2 Hospital, Ningbo 315010, Zhejiang, People's Republic of China. 2. Department of Orthopaedics Surgery, Ningbo No. 2 Hospital, Ningbo 315010, Zhejiang, People's Republic of China. Electronic address: pqjey@sina.com.
Abstract
BACKGROUND: Osteoarthritis (OA) is a degenerative joint disease that with the complication of disability, while inflammation is the important response of OA. MiR-149 was down-regulated in the OA tissues, while the potential mechanism of miR-149 in OA is unclear. METHODS: A total of 20 OA patients and 20 healthy persons were enrolled in the present study. Real-time PCR was used to detect miR-149 and the mRNA expression of TAK1, western blot was used to detect the protein expression of TAK1. Luciferase reporter assay was performed to identify the targeting relationship between miR-149 and TAK1. Elisa assay was used to identify the level of several pro-inflammatory cytokines. RESULTS: MiR-149 was down-regulated in both OA tissues and IL-1β-induced chondrocytes, while the expression of TAK1 was opposite. TAK1 was the target gene miR-149 targets TAK1 to regulate its expression. Human normal chondrocytes subjected to IL-1β significantly promoted the inflammatory response, and also accelerated the activation of NF-κB signaling pathway, while alternatively si-TAK1, miR-149 mimic or PDTC reversed the effects of IL-1β. Cells transfected with miR-149 inhibitor promotes the level of inflammation cytokines, as well as the activation of NF-κB, while cells co-transfected with si-TAK1 and miR-149 inhibitor abolishes the effects of miR-149 inhibitor. CONCLUSION: MiR-149 targets TAK1 to regulate the pathogenesis of OA, among which TAK1/NF-κB signaling acted as an important pathway in the inflammatory response that induced by IL-1β.
BACKGROUND:Osteoarthritis (OA) is a degenerative joint disease that with the complication of disability, while inflammation is the important response of OA. MiR-149 was down-regulated in the OA tissues, while the potential mechanism of miR-149 in OA is unclear. METHODS: A total of 20 OA patients and 20 healthy persons were enrolled in the present study. Real-time PCR was used to detect miR-149 and the mRNA expression of TAK1, western blot was used to detect the protein expression of TAK1. Luciferase reporter assay was performed to identify the targeting relationship between miR-149 and TAK1. Elisa assay was used to identify the level of several pro-inflammatory cytokines. RESULTS:MiR-149 was down-regulated in both OA tissues and IL-1β-induced chondrocytes, while the expression of TAK1 was opposite. TAK1 was the target gene miR-149 targets TAK1 to regulate its expression. Human normal chondrocytes subjected to IL-1β significantly promoted the inflammatory response, and also accelerated the activation of NF-κB signaling pathway, while alternatively si-TAK1, miR-149 mimic or PDTC reversed the effects of IL-1β. Cells transfected with miR-149 inhibitor promotes the level of inflammation cytokines, as well as the activation of NF-κB, while cells co-transfected with si-TAK1 and miR-149 inhibitor abolishes the effects of miR-149 inhibitor. CONCLUSION:MiR-149 targets TAK1 to regulate the pathogenesis of OA, among which TAK1/NF-κB signaling acted as an important pathway in the inflammatory response that induced by IL-1β.
Authors: Eliana Lara-Barba; María Jesús Araya; Charlotte Nicole Hill; Felipe A Bustamante-Barrientos; Alexander Ortloff; Cynthia García; Felipe Galvez-Jiron; Carolina Pradenas; Noymar Luque-Campos; Gabriela Maita; Roberto Elizondo-Vega; Farida Djouad; Ana María Vega-Letter; Patricia Luz-Crawford Journal: Front Immunol Date: 2021-11-01 Impact factor: 7.561