MicroRNA-106b overexpression suppresses synovial inflammation and alleviates synovial damage in patients with rheumatoid arthritis.

Abstract

To explore the effect of miR-106b on synovial inflammation and damage in rheumatoid arthritis (RA) patients and further to investigate its possible mechanism. Quantitative real-time polymerase chain reaction, immunofluorescence, in situ hybridization, and immunohistochemistry assay were used to verify the levels of miR-106b and cytokines. Pearson's correlation analysis was conducted to examine bivariate relationship between miR-106b and cytokines or receptor activator of nuclear factor-κ B ligand (RANKL). Following the isolation of fibroblast-like synoviocytes (FLS), the cultured cells were separately transfected with or without miR-106b mimic. Thereafter, cell proliferation, invasion and migration were measured by Cell Counting Kit-8 assay and Transwell assay, respectively. Furthermore, concentration and expression of cytokines were separately detected by enzyme-linked immunosorbent assay and Western blot. Compared with osteoarthritis, RA patients had a lower level of miR-106b and higher levels of RANKL, tumour necrosis factor-a (TNF-a), and interleukin-6 (IL-6). The relative transcription of miR-106b level was negatively correlated to TNF-a, IL-6, and RNKAL levels in both patients (all P < 0.05). Furthermore, miR-106b overexpression suppressed cell proliferation, migration, and invasion capacity of RA-FLS. miR-106b overexpression suppresses synovial inflammation and alleviates synovial damage; thus, it may be served as a potential therapeutic target for RA patients.