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BK Ambati, J Ambati, AM Joussen, A Anand, WA Kuziel, AP Adamis; Corneal Neovascularization: Transient Inhibition by Genetic Ablation of CCR2 and Sustained Inhibition by CCR5 Ablation . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1740.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To determine if genetic ablation of the chemokine receptors CCR2 and CCR5 (involved in leukocyte and endothelial chemotaxis) may inhibit the development of corneal neovascularization. Methods: Wild-type C57BL/6J mice, as well as species-specific counterparts with targeted homozygous disruption of the CCR2 or CCR5 gene, underwent chemical and mechanical denudation of corneal and limbal epithelium. Corneas were harvested 2 and 4 weeks after injury. Neovascularization was quantified by CD31 immunostaining. Results: The mean percentages of neovascularized corneal area in control mice, CCR2 deficient mice, and CCR5 deficient mice 2 weeks after denudation were 58.3%, 38.8% (P=0.047), and 38.5% (P=0.05), respectively. At 4 weeks after denudation, the corresponding values were 67.6%, 62.8% (P=0.344), and 44.0% (P=0.028). Conclusion: Development of corneal neovascularization is inhibited in CCR2 and CCR5 deficient mice; this inhibition is sustained only in the latter.
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