ArticleArthritis research & therapy2007
Soluble Fas ligand inhibits angiogenesis in rheumatoid arthritis.
Article in Arthritis research & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- A systematic review of preclinical studies on the efficacy of taurine for the treatment of rheumatoid arthritis.Amino acids · 2021Pooled it
- Article
- Encapsulated Mesenchymal Stromal Cell Microbeads Promote Endogenous Regeneration of Osteoarthritic Cartilage Ex Vivo.Advanced healthcare materials · 2021Article
- Apoptosis, Autophagy, NETosis, Necroptosis, and Pyroptosis Mediated Programmed Cell Death as Targets for Innovative Therapy in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Decoy Receptor 3 Promotes Preosteoclast Cell Death via Reactive Oxygen Species-Induced Fas Ligand Expression and the IL-1Mediators of inflammation · 2020Article
- The Effect of Triptolide in Rheumatoid Arthritis: From Basic Research towards Clinical Translation.International journal of molecular sciences · 2018Review
- Dual Role of Fas/FasL-Mediated Signal in Peripheral Immune Tolerance.Frontiers in immunology · 2017Review
- MIF allele-dependent regulation of the MIF coreceptor CD44 and role in rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Triptolide Modulates TREM-1 Signal Pathway to Inhibit the Inflammatory Response in Rheumatoid Arthritis.International journal of molecular sciences · 2016Article
- Construction of a recombinant adenovirus vector expressing IL-18BP/IL-4 fusion gene and the anti-inflammatory effect induced by this gene on lipopolysaccharide-stimulated synovial fibroblasts.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010Article
- Angiogenesis in rheumatoid arthritis.Autoimmunity · 2009Review
- Angiogenesis and its targeting in rheumatoid arthritis.Vascular pharmacology · 2009Review
- Targeting Angiogenesis in Rheumatoid Arthritis.Current rheumatology reviews · 2008Article
- Protective potential of SCF for mice preimplantation embryos cultured in vitro in suboptimal conditions.Journal of assisted reproduction and genetics · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The characteristics of rheumatoid arthritis (RA) pathology include the infiltration of inflammatory leukocytes, the proliferation of synovial cells, and the presence of extensive angiogenesis, referred to as rheumatoid pannus. Fas ligand is critical to the homeostatic regulation of the immune response, but its role in the angiogenic process of RA remains to be defined. In this study, we investigated whether soluble Fas ligand (sFasL) induces synoviocyte apoptosis and regulates angiogenesis of endothelial cells in RA. The levels of sFasL were elevated in the synovial fluids of RA patients when compared to those of osteoarthritis (OA) patients, and they correlated inversely with vascular endothelial growth factor165 (VEGF165) concentrations. sFasL, ranging from 10 to 100 ng/ml, induced the apoptosis of RA fibroblast-like synoviocytes (FLS) in vitro, and thereby decreased VEGF165 production. In addition, sFasL inhibited VEGF165-induced migration and chemotaxis of endothelial cells to basal levels in a manner independent of the Fas-mediated cell death. sFasL dose-dependently suppressed the VEGF165-stimulated increase in pAkt expression in endothelial cells, which might be associated with its anti-migratory effect on endothelial cells. Moreover, sFasL strongly inhibited neovascularization in the Matrigel plug in vivo. Our data suggest that sFasL shows anti-angiogenic activity within RA joints not only by inducing apoptosis of VEGF165-producing cells but also by blocking VEGF165-induced migration of endothelial cells, independent of Fas-mediated apoptosis.
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