Abstract
BackgroundVision loss due to vascular disease of the retina is a leading cause of blindness in the world. Retinal angiomatous proliferation (RAP) is a subgroup of neovascular age-related macular degeneration (AMD), whereby abnormal blood vessels develop in the retina leading to debilitating vision loss and eventual blindness. The novel mouse strain, neoretinal vascularization 2 (NRV2), shows spontaneous fundus changes associated with abnormal neovascularization. The purpose of this study is to characterize the induction of pathologic angiogenesis in this mouse model.MethodsThe NRV2 mice were examined from postnatal day 12 (p12) to 3 months. The phenotypic changes within the retina were evaluated by fundus photography, fluorescein angiography, optical coherence tomography, and immunohistochemical and electron microscopic analysis. The pathological neovascularization was imaged by confocal microscopy and reconstructed using three-dimensional image analysis software.ResultsWe found that NRV2 mice develop multifocal retinal depigmentation in the posterior fundus. Depigmented lesions developed vascular leakage observed by fluorescein angiography. The spontaneous angiogenesis arose from the retinal vascular plexus at postnatal day (p)15 and extended toward retinal pigment epithelium (RPE). By three months of age, histological analysis revealed encapsulation of the neovascular lesion by the RPE in the photoreceptor cell layer and subretinal space.ConclusionsThe NRV2 mouse strain develops early neovascular lesions within the retina, which grow downward towards the RPE beginning at p15. This retinal neovascularization model mimics early stages of human retinal angiomatous proliferation (RAP) and will likely be a useful in elucidating targeted therapeutics for patients with ocular neovascular disease.
Highlights
Vision loss due to vascular disease of the retina is a leading cause of blindness in the world and affects all age groups
A subgroup of neovascular age-related macular degeneration (AMD) coined as retinal angiomatous proliferation (RAP) has been described where the disease starts as neovessels originating from the retinal vascular bed and grow towards the outer retina, forming choroidal neovascularization [7,8,9]
Vascular leakage was detected by fluorescein angiography (FA)
Summary
Vision loss due to vascular disease of the retina is a leading cause of blindness in the world and affects all age groups. The abnormal vessels originate from retinal vasculature and can form a retinal– choroidal anastomosis (RCA) with the choroidal vascular bed [1,2,3,4]. These blood vessels are immature and leaky, resulting in subretinal and intraretinal edema and hemorrhage, which leads to vision loss [1,5]. Retinal angiomatous proliferation (RAP) is a subgroup of neovascular age-related macular degeneration (AMD), whereby abnormal blood vessels develop in the retina leading to debilitating vision loss and eventual blindness. The purpose of this study is to characterize the induction of pathologic angiogenesis in this mouse model
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