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

Liu, L.; Chen, H.; Jiang, T.; He, D.

Modern Rheumatology 32(6): 1054-1063


ISSN/ISBN: 1439-7609
PMID: 34850088
Accession: 079473983

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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 (qRT-PCR), immunofluorescence, in situ hybridization and immunohistochemistry assay were separately used to verify the levels of miR-106b and cytokines in the synovial tissues of patients with RA or osteoarthritis (OA). Pearson correlation analysis was conducted to examine the bivariate relationship between miR-106b and cytokines or RANKL. Following the isolation and culture of fibroblast-like synoviocytes (FLS), the cells were transfected with lentivirus-mediated miR-106b mimic, miR-106b inhibitor, and negative control miR-106b mimic, respectively. Thereafter, cell proliferation was measured by Cell Counting Kit-8 assay, and cell invasion and migration capacity was assessed by Transwell assay. Furthermore, concentration and expression of cytokines were separately detected by Enzyme linked immunosorbent assay and Western blot. Compared with osteoarthritis, validation by qRT-PCR showed that RA patients had a lower level of miR-106b and higher levels of receptor activator of nuclear factor-κ B ligand (RANKL), tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6). Additionally, the scatter plot showed that the relative transcription of miR-106b level was negatively correlated to the level of TNF-a, IL-6, and RNKAL in the synovial tissues of both RA and OA patients (All P<0.05). Furthermore, miR-106b overexpression suppressed cell proliferation, migration and invasion capacity of human 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.