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Abstract
PurposeTo assess iris neovascularization by uveal puncture of the mouse eye and determine the role of angiogenic factors during iris neovascularization.MethodsUveal punctures were performed on BalbC mouse eyes to induce iris angiogenesis. VEGF-blockage was used as an anti-angiogenic treatment, while normoxia- and hypoxia-conditioned media from retinal pigment epithelium (RPE) cells was used as an angiogenic-inducer in this model. Iris vasculature was determined in vivo by noninvasive methods. Iris blood vessels were stained for platelet endothelial cell adhesion molecule-1 and vascular sprouts were counted as markers of angiogenesis. Expression of angiogenic and inflammatory factors in the puncture-induced model were determined by qPCR and western blot.ResultsPunctures led to increased neovascularization and sprouting of the iris. qPCR and protein analysis showed an increase of angiogenic factors, particularly in the plasminogen-activating receptor and inflammatory systems. VEGF-blockage partly reduced iris neovascularization, and treatment with hypoxia-conditioned RPE medium led to a statistically significant increase in iris neovascularization.ConclusionsThis study presents the first evidence of a puncture-induced iris angiogenesis model in the mouse. In a broader context, this novel in vivo model of neovascularization has the potential for noninvasive evaluation of angiogenesis modulating substances.
Highlights
In the eye, the iris is the most anterior portion of the uvea, which constitutes the ciliary body and choroid
Punctures led to increased neovascularization and sprouting of the iris. quantitative real-time RT-PCR (qPCR) and protein analysis showed an increase of angiogenic factors, in the plasminogen-activating receptor and inflammatory systems
This study presents the first evidence of a puncture-induced iris angiogenesis model in the mouse
Summary
The iris is the most anterior portion of the uvea, which constitutes the ciliary body and choroid. Plenty of anastomosis is found between arteries and veins [1], allowing nutrition and oxygen supply to the iris tissue and to the anterior chamber of the eye, and maintain intraocular homeostasis [2]. The development of the eye is not final at birth. Mouse ocular vasculature development continues after birth with mice pups opening their eyes approximately 12.5 days after birth [3,4]. As such, induced angiogenesis models in the mouse eye, as is the example of oxygen-induced retinopathy (OIR), a model of retinopathy of prematurity, have been established based on these developmental characteristics [5]
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