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Peirong Lu, Longbiao Li, Gaoqin Liu, Xueguang Zhang, Naofumi Mukaida; Enhanced Experimental Corneal Neovascularization along with Aberrant Angiogenic Factor Expression in the Absence of IL-1 Receptor Antagonist. Invest. Ophthalmol. Vis. Sci. 2009;50(10):4761-4768. doi: 10.1167/iovs.08-2732.
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purpose. To address the roles of the endogenously produced IL-1ra in the course of corneal neovascularization (CNV).
methods. CNV was induced by alkali injury and compared in wild-type (WT), IL-1 receptor antagonist (ra) knockout (KO) mice and anti–IL-1ra antibody-treated WT mice 2 weeks after injury. Angiogenic factor expression and leukocyte accumulation in the early phase after injury were quantified by RT-PCR and immunohistochemical analysis, respectively.
results. The mRNA expression of IL-1ra, IL-1α, and IL-1β was augmented, together with infiltration of F4/80+ macrophages and Gr-1+ neutrophils, in corneas after alkali injury. Intracorneally infiltrating macrophages, but not neutrophils, expressed IL-1ra. Compared with WT mice, either IL-1ra KO mice or anti–IL-1ra antibody-treated WT mice exhibited enhanced CNV 2 weeks after injury, as evidenced by enlarged CD31+ areas. Concomitantly, the infiltration of F4/80+ macrophages was more significantly enhanced in IL-1ra KO mice than in WT mice. Intraocular mRNA expression enhancement of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) was greater in IL-1ra KO mice than in WT mice after injury. Moreover, IL-1α and IL-1β enhanced VEGF and iNOS expression by murine peritoneal macrophages.
conclusions. IL-1ra KO exhibited enhanced alkali-induced CNV through enhanced intracorneal macrophage infiltration and increased expression of VEGF and iNOS.
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