Affiliation:
1. Department of Rheumatology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China
2. Department of Rheumatology, Shanghai Guanghua Hospital of Integrated Traditional and Western Medicine, Shanghai, China
3. Arthritis Institute of Integrated Traditional and Western Medicine, Shanghai Chinese Medicine Research Institute, Shanghai, China
Abstract
ABSTRACT
Objectives
To explore the effect of miR-106b on synovial inflammation and damage in rheumatoid arthritis (RA) patients and further to investigate its possible mechanism.
Methods
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.
Results
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.
Conclusions
miR-106b overexpression suppresses synovial inflammation and alleviates synovial damage; thus, it may be served as a potential therapeutic target for RA patients.
Publisher
Oxford University Press (OUP)
Cited by
6 articles.
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