Upregulating miR‑27a‑3p inhibits cell proliferation and inflammation of rheumatoid arthritis synovial fibroblasts through targeting toll‑like receptor 5
- Lifeng Chen
- Qiping Lu
- Jianhua Chen
- Ruibing Feng
- Chenxi Yang
Affiliations: Department of Rheumatology and Immunology, General Hospital of Central Theater Command, Wuhan, Hubei 430070, P.R. China, Department of General Surgery, General Hospital of Central Theater Command, Wuhan, Hubei 430070, P.R. China, Department of Orthopedics, Central People's Liberation Army Central Theater, Wuhan, Hubei 430070, P.R. China, Department of Orthopedics, Graduate School of Hubei University of Traditional Chinese Medicine, Wuhan, Hubei 430061, P.R. China
- Published online on: August 27, 2021 https://doi.org/10.3892/etm.2021.10661
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Rheumatoid arthritis (RA) is a serious chronic inflammatory disease and synovial fibroblasts (SFs) serve a vital role in the pathogenesis and progression of RA. Current studies have demonstrated that dysregulation of microRNAs is involved in RA etiopathogenesis. The present study aimed to investigate the role of microRNA (miR)‑27a‑3p in RASFs, as well as its molecular mechanism. RASFs were isolated from synovial tissues from patients with RA. Expression of miR‑27a‑3p and toll‑like receptor 5 (TLR5) was detected using reverse transcription‑quantitative polymerase chain reaction and western blotting. Cell proliferation, apoptosis and inflammatory response were measured with MTT assay, flow cytometry and ELISA kits, respectively. The target binding between miR‑27a‑3p and TLR5 was predicted on DIANA TOOLS software, and confirmed by dual‑luciferase reporter assay and Biotin‑coupled miRNA pull‑down assay. Expression of miR‑27a‑3p was downregulated and TLR5 was upregulated in synovial tissues and RASFs isolated from patients with RA. Functionally, upregulating miR‑27a‑3p may promote the apoptosis rate of RASFs and suppress cell proliferation and secretions of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α. TLR5 was validated as a downstream target for miR‑27a‑3p in RASFs, and its expression was negatively regulated by miR‑27a‑3p. Silencing TLR5 in RASFs may exert similar effects to miR‑27a‑3p‑overexpression; whereas, restoring TLR5 counteracted the suppression of miR‑27a‑3p‑overexpression on RASF proliferation and inflammation, as well as the promotion on apoptosis. miR‑27a‑3p upregulation may suppress RA progression by inhibiting RASFs proliferation and inflammation through targeting TLR5.