Basic & Clinical Medicine ›› 2020, Vol. 40 ›› Issue (1): 9-15.

• Original Articles • Previous Articles     Next Articles

Effect of miR-29a on proliferation and apoptosis of fibroblast-like synoviocyte in rheumatoid arthritis

GUO Xiong-fei*, WANG Ting, TANG Li-xin   

  1. Department of Orthopaedics, Nanyang Central Hospital, the Affiliated Nanyang Hospital, Zhengzhou University, Nanyang 473000, China
  • Received:2019-04-03 Revised:2019-07-08 Online:2020-01-05 Published:2019-12-27
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Abstract: Objective To investigate the effect of miR-29a on the activity and apoptosis of fibroblast-like synoviocyte(FLS) in rheumatoid arthritis(RA). Methods The normal human FLS (n-FLS) and RA patients FLS (RA-FLS) were isolated and cultured,and the expression level of CHI3L1 protein was detected by Western blot. miR-29a mimics, si-NFAT5 and miR- 29a+NFAT5 were transfected into RA-FLS for 48 h. Then,the expression levels of miR-29a and NFAT5 mRNA were detected by RT-qPCR, the cell viability and apoptosis were detected by MTT assay and flow cytometry,respectively and the expression of p38, p-p38, cleaved-caspase3 proteins were detected by Western blot. Targeting relationship between miR-29a and NFAT5 was validated by dual fluorescent reporter gene detection system. Results Compared with n-FLS, the expression level of CHI3L1 protein in RA-FLS was increased significantly (P<0.05). After over-expression of miR-29a or inhibition of NFAT5, the cell viability decreased, the apoptosis rate increased, the expression of p-p38 decreased, and the expression of cleaved-caspase3 increased significantly(P<0.05). Luciferase activity of RA-FLS was significantly decreased in miR-29a and wild-type NFAT5 3′UTR co-transfection group, but increased in anti-miR-29a and wild-type NFAT5 3′UTR co-transfection group (P<0.05). Over-expression of miR-29a significantly decreased the expression of NFAT5, and inhibition of miR-29a significantly increased the expression of NFAT5 (P<0.05).Over-expression of NFAT5 can weaken the effect of over-expression of miR-29a on RA-FLS activity and apoptosis (P<0.05). Conclusions miR-29a can inhibit the activity of RA-FLS and induce its apoptosis by targeting NFAT5 to down-regulate p38 MAPK signaling pathway.

Key words: rheumatoid arthritis(RA), fibroblast-like synoviocyte(FLS), miR-29a target gene, nuclear factor of activated T cells 5(NFAT5), p38MAPK signaling pathway

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