MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression
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 eva...
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Published in: | Archives of rheumatology Vol. 38; no. 1; pp. 119 - 128 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Istanbul
Turkish League Against Rheumatism
01-03-2023
Prof Sebnem Ataman, President Turkish League Against Rheumatism |
Subjects: | |
Online Access: | Get full text |
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Summary: | 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-2'-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. Keywords: Atl2, fibroblast-like synoviocytes, inflammatory response, MiR-30e-5p, rheumatoid arthritis. |
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ISSN: | 2148-5046 1309-0291 2618-6500 1309-0283 |
DOI: | 10.46497/ArchRheumatol.2023.9526 |