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      Angiogenesis mediated by soluble forms of E-selectin and vascular cell adhesion molecule-1.

      Nature
      Animals, Antigens, CD15, physiology, Arthritis, Rheumatoid, complications, metabolism, Cell Adhesion, Cell Adhesion Molecules, Chemotaxis, Cornea, cytology, E-Selectin, Endothelium, Vascular, Humans, Neovascularization, Pathologic, etiology, Rats, Recombinant Proteins, Solubility, Synovial Fluid, Vascular Cell Adhesion Molecule-1

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          Abstract

          Endothelial adhesion molecules facilitate the entry of leukocytes into inflamed tissues. This in turn promotes neovascularization, a process central to the progression of rheumatoid arthritis, tumor growth and wound repair. Here we test the hypothesis that soluble endothelial adhesion molecules promote angiogenesis. Human recombinant soluble E-selectin and soluble vascular cell adhesion molecule-1 induced chemotaxis of human endothelial cells in vitro and were angiogenic in rat cornea. Soluble E-selectin acted on endothelial cells in part through a sialyl Lewis-X-dependent mechanism, while soluble vascular cell adhesion molecule-1 acted on endothelial cells in part through a very late antigen (VLA)-4 dependent mechanism. The chemotactic activity of rheumatoid synovial fluid for endothelial cells, and also its angiogenic activity, were blocked by antibodies to either soluble E-selectin or soluble vascular cell adhesion molecule-1. These results suggest a novel function for soluble endothelial adhesion molecules as mediators of angiogenesis.

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