MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression
Department of Rheumatology, the Affiliated Huaian No. 1 People’s Hospital of Nanjing Medical University, Huaian, China
Keywords: Atl2, fibroblast-like synoviocytes, inflammatory response, MiR-30e-5p, rheumatoid arthritis.
Objectives: This study aims to investigate the inflammatory effect of the microRNA (miRNA) miR-30e-5p on rheumatoid arthritis (RA) development in RA mice and fibroblast-like synoviocytes (FLS).
Materials and methods: MiR-30e-5p and atlastin GTPase 2 (Atl2) expression in RA tissues and RA-FLS was evaluated using real-time quantitative polymerase chain reaction. The function of miR-30e-5p in inflammation of RA mice and RA-FLS was analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blotting. 5-ethynyl-2ˊ-deoxyuridine (EdU) assay was used to detect RA-FLS proliferation. Luciferase reporter assay was to confirm the interaction between miR-30e-5p and Atl2.
Results: MiR-30e-5p expression was upregulated in the tissues from RA mice. Silencing miR-30e-5p alleviated inflammation in RA mice and RA-FLS. MiR-30e-5p negatively modulated Atl2 expression. Atl2 knockdown exerted a proinflammatory effect on RA-FLS. Atl2 knockdown rescued the inhibitory effect of miR-30e-5p knockdown on proliferation and inflammatory response of RA-FLS.
Conclusion: MiR-30e-5p knockdown inhibited the inflammatory response in RA mice and RA-FLS through Atl2.
*These authors contributed equally to the work.
Citation: Liu S, Wang K, Li J, Liu Y, Zhang Z, Meng D. MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression. Arch Rheumatol 2023;38(1):119-128.
The study protocol was approved by the Wuhan Hualian ke Biology Technology Co., Ltd. Ethics Review Committee (date: 05.05.2021, no: 202105006). The study was conducted in accordance with the principles of the Declaration of Helsinki.
Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Idea/concept: S.L.; Design, critical review: S.L.; K.W.; Control/supervision, data collection and/or processing: J.L.; Analysis and/or interpretation: Y.L.; Literature review, writing the article: Z.Z., D.M.; References and fundings, materials: J.L., Y.L.
The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.
The authors received no financial support for the research and/or authorship of this article.