Abstract
Background: Rheumatoid arthritis (RA) is a inflammatory disease that characterized with the destruction of synovial joint, which could induce disability. Inflammatory response mediated the RA. It has been reported that MiR-128-3p is significantly increased in RA, while the potential role was still unclear.Methods: T cells in peripheral blood mononuclear cell (PBMC) were isolated from the peripheral blood from people of RA and normal person were used. Real-time PCR was performed to detect the expression of MiR-128-3p, while the protein expression of tumor necrosis factor-α-induced protein 3 (TNFAIP3) was determined using Western blot. The levels of IL-6 and IL-17 were measured using enzyme-linked immunosorbent assay (ELISA). The expression of CD69 and CD25 was detected using flow cytometry. The RA mouse model was constructed for verification of the role of MiR-128-3p.Results: The expression of MiR-128-3p was significantly increased, while TNFAIP3 was decreased, the levels of IL-6 and IL-17 were also increased in the T cells of RA patients. Down-regulated MiR-128-3p significantly suppressed the expression of p-IkBα and CD69, and CD25in T cells. MiR-128-3p targets TNFAIP3 to regulate its expression. MiR-128-3p knockdown significantly suppressed the activity of nuclear factor κB (NF-κB) and T cells by up-regulating TNFAIP3, while cells co-transfected with si-TNFAIP3 abolished the effects of MiR-128-3p knockdown. The in vivo experiments verified the potential role of MiR-128-3p on RA.Conclusion: Down-regulated MiR-128-3p significantly suppressed the inflammation response of RA through suppressing the activity of NF-κB pathway, which was mediated by TNFAIP3.
Highlights
Rheumatoid arthritis (RA) is a inflammatory disease that characterized with the destruction of synovial joints, which severely threatens human joint
The cytokines of IL-6 and IL-17 were markedly higher in RA patients rather than in control (Figure 1C)
We found that the inflammatory cytokines IL-6 and IL-17 were significantly increased in T cells of RA, knockdown of MiR-128-3p significantly decreased the levels of IL-6 and IL-17, while cells co-transfected with MiR-128-3p inhibitor and si-tumor necrosis factor-α-induced protein 3 (TNFAIP3) abolished the effects of MiR-128-3p inhibitor, indicating that MiR-128-3p regulated the inflammatory response of RA is through regulating the expression of TNFAIP
Summary
Rheumatoid arthritis (RA) is a inflammatory disease that characterized with the destruction of synovial joints, which severely threatens human joint. The nuclear factor κB (NF-κB), a transcription factor, is involved in the inflammatory process of RA, and the NF-κB signaling pathway has been reported to conduct the c 2018 The Author(s). Results: The expression of MiR-128-3p was significantly increased, while TNFAIP3 was decreased, the levels of IL-6 and IL-17 were increased in the T cells of RA patients. Down-regulated MiR-128-3p significantly suppressed the expression of p-IkBα and CD69, and CD25in T cells. MiR-128-3p knockdown significantly suppressed the activity of nuclear factor κB (NF-κB) and T cells by up-regulating TNFAIP3, while cells co-transfected with si-TNFAIP3 abolished the effects of MiR-128-3p knockdown. Conclusion: Down-regulated MiR-128-3p significantly suppressed the inflammation response of RA through suppressing the activity of NF-κB pathway, which was mediated by TNFAIP3
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