Expression and function of miR‑155 in rat synovial fibroblast model of rheumatoid arthritis

Li,Hewei; Liu,Ping; Gong,Yanlin; Liu,Jiali; Ruan,Feng

doi:10.3892/etm.2019.7581

Expression and function of miR‑155 in rat synovial fibroblast model of rheumatoid arthritis

Authors:
- Hewei Li
- Ping Liu
- Yanlin Gong
- Jiali Liu
- Feng Ruan
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Affiliations: Department of Orthopedics, Liyuan Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430077, P.R. China, Department of Endocrinology, Wuhan No. 1 Hospital, Wuhan, Hubei 430022, P.R. China
Published online on: May 15, 2019 https://doi.org/10.3892/etm.2019.7581
Pages: 786-792
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Rheumatoid arthritis (RA) is a common autoimmune disease characterized by joint synovial inﬂammation and is a challenge for researchers and clinicians. MicroRNAs (miRNAs/miRs) represent a group of small non‑coding RNA molecules that post‑transcriptionally regulate mRNA expression and are involved in various diseases, including cancer, autoimmune and metabolic diseases, as well as neurological disorders. In the present study, various experiments were performed to investigate the effects and underlying mechanism of miR‑155 in RA using rat synoviocytes induced by lipopolysaccharide (LPS) to model rheumatoid arthritis. It was revealed that synovial fibroblasts exhibited significantly higher miR‑155 mRNA levels than the control group. Compared with the RA group, the viability of synovial fibroblasts was significantly decreased in the miR‑155 mimics + RA group, but markedly increased in the miR‑155 inhibitor + RA group. Compared with that in the RA + NC mimic or RA + NC inhibitor groups, the apoptosis of synovial fibroblasts increased significantly in the miR‑155 mimics + RA group, but was significantly decreased in the miR‑155 inhibitor + RA group. The miR‑155 mimics + RA group exhibited higher expression levels of β‑catenin, matrix metalloproteinase 7 and cyclin D1 compared with the miR‑155 inhibitor + RA group, and the glycogen synthase kinase protein levels was lower compared with the miR‑155 inhibitor + RA group. In brief, it was inferred that the Wnt signaling pathway is involved in the miR‑155‑associated inhibition of RA synovial fibroblast viability and induction of cell apoptosis. Inhibition of miR‑155 may be an effective treatment for RA through regulation of the Wnt signaling pathway to reduce cell apoptosis and enhance cell viability.

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