Abstract

Aim: To discuss TRIM3’s effects and relative mechanisms in RA development. Materials and methods: Using FLS as research object in our study. Present study divided into two steps, first step, discussing TRIM3 depressing effects in normal FLS cell; next, using IL-1β stimulating to make RA cell model, TRIM3 overexpression in RA model to observe cell biological activities. Measuring IL-6 and TNF-α levels by ELISA kit; evaluating cell proliferation by MTT and EdU assay; relative proteins including TRIM3, TAB2 and NF-κB(p65) proteins expression using WB method. Results: With TRIM3 knockdown, FLS cell proliferation were significantly increased with IL-6, TNF-α levels significantly up-regulation (P < 0.001, respectively). Meanwhile, TAB2 protein expression significantly depressing and NF-κB(p65) protein significantly increasing; those were similar as IL-1β stimulating RA cell model in FLS cell line. In RA cell model, transfection TRIM3 in FLS cell, the cell proliferation was significantly depressed with IL-1β, TNF-α levels depressing, and TAB2 protein expression significantly increasing and NF-κB(p65) protein significantly depressing. Conclusion: TRIM3 knockdown might be a result to RA development; with TRIM3 overexpression, RA induced FLS hyperproliferation significantly improved with TAB2 up-regulation and NF-κB(p65) down-regulation in vitro.

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