AB0099 Overexpression of uPAR in Fibroblast-like Synoviocytes Promotes Angiogenesis in Patients with Rheumatoid Arthritis. (15th July 2016)
- Record Type:
- Journal Article
- Title:
- AB0099 Overexpression of uPAR in Fibroblast-like Synoviocytes Promotes Angiogenesis in Patients with Rheumatoid Arthritis. (15th July 2016)
- Main Title:
- AB0099 Overexpression of uPAR in Fibroblast-like Synoviocytes Promotes Angiogenesis in Patients with Rheumatoid Arthritis
- Authors:
- Yan, L.
Feng, P.Y.
Ting, W.Y.
Meng, L. - Abstract:
- Abstract : 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. References: NohAbstract : 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. References: Noh H, Hong S, Huang S. Role of urokinase receptor in tumor progression and development. Theranostics. 2013;3(7):487–95. Ferraris GM, Sidenius N. Urokinase plasminogen activator receptor: a functional integrator of extracellular proteolysis, cell adhesion, and signal transduction. Seminars in thrombosis and hemostasis. 2013;39(4):347–55. Yoo SA, Kwok SK, Kim WU. Proinflammatory role of vascular endothelial growth factor inthe pathogenesis of rheumatoid arthritis: prospects for therapeutic intervention. Mediators of inflammation. 2008;2008:129873. Disclosure of Interest: None declared … (more)
- Is Part Of:
- Annals of the rheumatic diseases. Volume 75(2016)Supplement 2
- Journal:
- Annals of the rheumatic diseases
- Issue:
- Volume 75(2016)Supplement 2
- Issue Display:
- Volume 75, Issue 2 (2016)
- Year:
- 2016
- Volume:
- 75
- Issue:
- 2
- Issue Sort Value:
- 2016-0075-0002-0000
- Page Start:
- 930
- Page End:
- 931
- Publication Date:
- 2016-07-15
- Subjects:
- Rheumatism -- Periodicals
616.723005 - Journal URLs:
- http://ard.bmjjournals.com/ ↗
http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=149&action=archive ↗
http://www.bmj.com/archive ↗
http://gateway.ovid.com/server3/ovidweb.cgi?T=JS&MODE=ovid&D=ovft&PAGE=titles&SEARCH=annals+of+the+rheumatic+diseases.tj&NEWS=N ↗ - DOI:
- 10.1136/annrheumdis-2016-eular.5155 ↗
- Languages:
- English
- ISSNs:
- 0003-4967
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - BLDSS-3PM
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- 18014.xml