Decreased MiR-128-3p alleviates the progression of rheumatoid arthritis by up-regulating the expression of TNFAIP3

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.

Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

“…Furthermore, a decreased miR-128-3p level was observed in ox-LDL-induced cells. The present evidence suggests that miR-128-3p is a tumor suppressor in human diseases, including glioma, 30 esophageal squamous-cell cancer, 31 rheumatoid arthritis, 32 and hepatocellular carcinoma. 33 Moreover, miR-128 knockdown regulated by lncRNA NEAT1 leads to ox-LDL-regulated inammation and oxidative stress.…”

<p>Long Noncoding RNA SNHG16 Sponges miR-182-5p And miR-128-3p To Promote Retinoblastoma Cell Migration And Invasion By Targeting LASP1</p>

“…For example, miR-128-3p inhibits metastasis and EMT by targeting ZEB1 in esophageal squamous cell cancer, reduces the migration and invasion ability of glioma cell through regulating GREM1 and suppresses osteosarcoma proliferation and metastasis by reducing VEGFC 27–29. miR-128-3p also plays a key role in regulating the development and progression of rheumatoid arthritis, type 2 diabetes and atrial fibrillation 30–32…”

MiR-128-3p Post-Transcriptionally Inhibits WISP1 to Suppress Apoptosis and Inflammation in Human Articular Chondrocytes via the PI3K/AKT/NF-κB Signaling Pathway

“…In addition, overexpression of miR-128 enhanced the expression of genes involved in inflammation, proinflammatory cytokines, and fibrosis in normal rat kidney cells 19 . Downregulation of miR-128-3p significantly inhibited the inflammatory response of rheumatoid arthritis by targeting TNFAIP3 to inhibit the activity of the NF-κB pathway 13 . Considering the role of miR-128 in disease progression is controversial, we investigated the role of miR-128 in the development of OA.…”