Affiliation:
1. Department of Rheumatology, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, P. R. China
2. Center of Clinical Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, 215000, Jiangsu, P. R. China
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.
Publisher
American Scientific Publishers
Subject
Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology