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I.C. Van der Ploeg, B. Samolov, M. Aronsson, A. Kvanta; Delayed Corneal Neovascularization in IL–10–Deficient C57BL/6 Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1627.
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© ARVO (1962-2015); The Authors (2016-present)
To elucidate the importance of the anti–inflammatory cytokine IL–10 for inflammation induced angiogenesis in an experimental model for corneal neovascularization.
A suture model was used to induce corneal angiogenesis in IL–10 –/– and wild–type C57BL/6 mice. The quantitative comparison of neovascularization was performed by measurements of neovascularized areas on corneal flat–mounts. Immunohistochemistry was used to characterize the inflammatory response and to co–visualize hemangiogenesis and lymphangiogenesis. mRNA expression for IL–10, metalloproteinase–2 (MMP–2), MMP–9 and vascular endothelial growth factor–A (VEGF–A) was detected by real–time RT–PCR.
IL–10 –/– mice showed a delayed neovascular response compared to wild–type animals. This quantitative difference reached statistical significance 6 days after suture, when approximately one half of the cornea was neovascularized and IL–10 mRNA expression showed its peak. No significant differences in mRNA expression for VEGFA, MMP–2 or MMP–9 were detected day 6 in IL–10 –/– versus wild–type mice. Angiogenesis was accompanied by lymphangiogenesis and a pronounced inflammatory response in both IL–10 –/– and wild–type animals, with no striking differences between the groups.
IL–10 has a pro–angiogenic effect in the suture model for corneal neovascularization that can neither be explained by IL–10s anti–inflammatory effect nor by apparent cross–talk with proangiogenic factors such as VEGF–A, MMP–2 and MMP–9.
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