Inhibition of angiogenesis in rats by IL-1 receptor antagonist and selected cytokine antibodies.
Daily administration of 50 ng recombinant human interleukin 1-alpha ( IL-1 alpha), 25 ng IL-8, 50 ng tumor necrosis factor-alpha ( TNF-alpha), or 100 ng basic fibroblast growth factor ( bFGF) caused intense neovascularization in a rat sponge model. These cytokine-induced neovascular responses were inhibited by coadministration of IL-1 receptor antagonist (IL-1ra; 50 micrograms), IL-8 antiserum (IL-8-AS; 1: 1000), TNF-alpha antibody (TNF-AB; 500 ng), or a monoclonal antibody to bFGF ( DG2; 1000 ng), respectively. These data suggest that it is possible to manipulate the angiogenic response elicited by a defined cytokine by its receptor antagonist or neutralizing antibody. In the absence of exogenous cytokines, the sponge-induced angiogenesis was profoundly suppressed by dexamethasone (5 micrograms/day), but not modified by IL-1ra, IL-8-AS, TNF-AB, and DG2 alone. However, the combination of these four reagents was able to inhibit the sponge-induced neovascular response almost completely. These findings provide direct evidence that IL-1 alpha, IL-8, TNF-alpha and/or bFGF have an intrinsic role in angiogenesis. Further work is necessary to characterize the profile of these cytokines during angiogenesis and to elucidate the nature of their interactions.[1]References
- Inhibition of angiogenesis in rats by IL-1 receptor antagonist and selected cytokine antibodies. Hu, D.E., Hori, Y., Presta, M., Gresham, G.A., Fan, T.P. Inflammation (1994) [Pubmed]
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