MiR-30e-5p deficiency exerts an inhibitory effect on inflammation in rheumatoid arthritis via regulating Atl2 expression

MiR-30e-5p 缺陷通过调节 Atl2 表达对类风湿关节炎的炎症产生抑制作用

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作者:Shanshan Liu, Kai Wang, Ju Li, Yan Liu, Zhongyuan Zhang, Deqian Meng

Conclusion

MiR-30e-5p knockdown inhibited the inflammatory response in RA mice and RA-FLS through Atl2.

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.

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