Background Urokinase-type plasminogen activator receptor (uPAR), is a multi-functional receptor on cell surface, widely present in endothelial cells, fibroblasts, and a variety of malignant cells. Our previous studies have suggested that expression of uPAR is higher in patients with rheumatoid arthritis (RA) compared to osteoarthritis (OA) and the traumatic patients.
Objectives Our objective was to investigate the promoting-angiogenesis effects of uPAR in fibroblast-like synoviocytes from patients with rheumatoid arthritis (RA-FLSs).
Methods Chemically synthesized small interference RNA (siRNA) specifically targeting the uPAR gene was transfected into RA-FLSs by cationic liposome and the cell supernatants from uPAR gene-silenced RA-FLSs were extracted to cultivate the EA.hy926 (a human endothelial cell line). Transwell and tubule formation assays were used to explore the influence of RA-FLSs uPAR on EA.hy926 angiogenesis.
Results EA.hy926 cells treated with conditioned medium of uPAR-siRNA RA-FLSs had a worse migrating ability and tubule formation effects, for they had only about 38% transmembrane cells and the average number of complete tubular structures decreased to 38.2%,relative to the transfection reagent control group (*P<0.05).
Conclusions uPAR in RA-FLSs affects neoangiogenesis of synovial tissues in patients with RA, which imply that targeting uPAR and its downstream signal pathway may provide beneficial therapeutic effects on RA.
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Disclosure of Interest None declared
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