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T Usui, Y Kaji, K Yamashiro, S Ishida, JM Isner, T Asahara, AP Adamis; ICAM-1/CD18 Dependent Recruitment of Endothelial Progenitor Cells to Sites of Inflammatory Corneal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1763.
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Purpose:Inflammation and neovascularization frequently co-exist in disease. Studies aimed at inhibiting inflammation, whether through leukocyte depletion or adhesion molecule inhibition, have demonstrated a causal role for "leukocytes" in pathological neovascularization. The current study investigated the mechanistic link between the leukocyte adhesion molecules ICAM-1 and CD18, and the recruitment of circulating endothelial progenitor cells (EPC) to sites of pathological adult corneal neovascularization. Methods:Corneal neovascularization was induced in mice following bone marrow transplants expressing the b-galactosidase gene under the transcriptional control of the endothelial specific promotor Tie2. Results:Following the induction of corneal neovascularization, EPC appeared in the corneal stroma and were incorporated within the growing vasculature. When neutralizing CD18 and ICAM-1 antibodies were administered systemically, corneal neovascularization and corneal EPC density were both suppressed. Immunofluorescence studies revealed the presence of CD18 on EPC, and in vitro adhesion assays demonstrated that the antibody-based neutralization of CD18 suppresses the binding of EPC to endothelial cell monolayers. Conclusion:Taken together, these data demonstrate that circulating EPC arrive at sites of neovascularization via the leukocyte adhesion molecules CD18 and ICAM-1, and explain, in part, why "leukocyte" inhibition suppresses pathological adult neovascularization.
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