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• W2154583934 abstract "Abstract Angiogenesis is an early and a critical event in the pathogenesis of rheumatoid arthritis (RA). Neovascularization is dependent on endothelial cell activation, migration and proliferation, and inhibition of angiogenesis may provide a novel therapeutic approach in RA. In this study, we document a novel role of IL-17 in mediating angiogenesis. Local expression of IL-17 in mouse ankles increases vascularity. We further demonstrate that IL-17 is angiogenic by showing its ability to promote blood vessel growth in Matrigel plugs in vivo. Additionally, IL-17, in concentrations present in the RA joint, induces human lung microvascular endothelial cell (HMVEC) migration mediated through the PI3K/AKT1 pathway. Furthermore, suppression of the PI3K pathway markedly reduces IL-17–induced tube formation. We also show that both IL-17–induced HMVEC chemotaxis and tube formation are mediated primarily through IL-17 receptor C. Neutralization of either IL-17 in RA synovial fluids or IL-17 receptor C on HMVECs significantly reduces the induction of HMVEC migration by RA synovial fluid. Finally, RA synovial fluid immunoneutralized with anti–IL-17 and antivascular endothelial growth factor does not reduce HMVEC migration beyond the effect detected by immunodepleting each factor alone. These observations identify a novel function for IL-17 as an angiogenic mediator in RA, supporting IL-17 as a therapeutic target in RA." @default.
• W2154583934 created "2016-06-24" @default.
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• W2154583934 date "2010-03-15" @default.
• W2154583934 modified "2023-10-11" @default.
• W2154583934 title "IL-17 Contributes to Angiogenesis in Rheumatoid Arthritis" @default.
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• W2154583934 doi "https://doi.org/10.4049/jimmunol.0903271" @default.
• W2154583934 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2857761" @default.
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• W2154583934 hasPublicationYear "2010" @default.
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