IFITM3对类风湿关节炎滑膜成纤维细胞功能影响的研究OA

Objective:To investigate the effect of IFITM3 on the function of synovial fibroblasts in rheumatoid arthritis.Meth-ods:In vitro cell models of RA-FLSs were constructed,and the protein expression differences of IFITM3 in RA-FLSs were de-tected by Western blot.The experiments were divided into the Control group,the LPS group,the LPS+siNC group,the LPS+siIFITM3 group,and the LPS+siIFITM3+C16-PAF group.Transwell test and scratch test were used to observe the changes in the invasion and migration ability of RA-FLSs,respectively.The levels of TNF-α,IL-1 and IL-6 were detected by ELISA.Flow cytometry was used to detect the apoptosis of RA-FLSs.CCK8 was used to detect cell proliferation.The mRNA expressions of IFITM3,Bax and Bcl-2 were detected by real-time PCR.Western blot was used to detect the protein expressions of IFITM3,MEK,ERK,p-ERK1/2,MMP9,Bax and Bcl-2.In the IFITM3 siRNA panel,the MER/ERK signaling pathway was activated with C16-PAF,and cell proliferation was detected with CCK8.Results:In this study,the expression level of IFITM3 in LPS-treated RA-FLSs was increased(P<0.05).Compared to the LPS group and the LPS+siNC group,the migration ability and invasion ability of RA-FLSs cells in the LPS+siIFITM3 group decreased,the apoptosis rate increased,the expression of in-flammatory cytokines IL-1,IL-6 decreased,and the cell proliferation activity decreased(P<0.05).The expression of Bax in-creased and the expression of Bcl-2,p-ERK and MMP9 decreased(P<0.05).Compared to the LPS+siIFITM3 group,the pro-liferative activity of RA-FLSs in the LPS+si-IFITM3+C16-PAF group was increased(P<0.05).Conclusion:Down-regulation of IFITM3 can inhibit the migration and invasion ability of RA-FLSs,the expression of inflammatory cytokines IL-1 and IL-6,in-hibit proliferation and promote apoptosis.The mechanism of regulation of proliferation may be related to the level of MEK/ERK signal activation.