ArticleInvestigative ophthalmology & visual science2013
A murine model for retinopathy of prematurity identifies endothelial cell proliferation as a potential mechanism for plus disease.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 25 citations in OpenAlex.
- Application of a Quantitative Vascular Severity Score in Retinopathy of Prematurity in the United States and India: New Insights Into Disease Epidemiology and Pathophysiology.American journal of ophthalmology · 2026Article
- Characterization of vascular tortuosity throughout the murine oxygen-induced retinopathy model of ischemic retinopathy.JCI insight · 2026Article
- Targeting ATF6 reduces pathological neovascularization and improves visual outcomes in retinal disease models.Scientific reports · 2025Article
- The Role of ADAM9 and MMP9 in Diabetic Retinopathy: Insights from Ocular Parameters.International journal of molecular sciences · 2025Article
- Reduction of pathological retinal neovascularization, vessel obliteration, and artery tortuosity by PEDF protein in an oxygen-induced ischemic retinopathy rat model.FASEB bioAdvances · 2024Article
- Retinopathy of prematurity: contribution of inflammatory and genetic factors.Molecular and cellular biochemistry · 2022Review
- An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases.International journal of molecular sciences · 2020Review
- Hyperoxia affects the lung tissue: A porcine histopathological and metabolite study using five hours of apneic oxygenation.Metabolism open · 2019Article
- Metalloproteinases mediate diabetes-induced retinal neuropathy and vasculopathy.Cellular and molecular life sciences : CMLS · 2019Review
- The genetics of retinopathy of prematurity: a model for neovascular retinal disease.Ophthalmology. Retina · 2018Article
- An apelin receptor antagonist prevents pathological retinal angiogenesis with ischemic retinopathy in mice.Scientific reports · 2017Article
- In Vivo Angiography Quantifies Oxygen-Induced Retinopathy Vascular Recovery.Optometry and vision science : official publication of the American Academy of Optometry · 2016Article
- The Eyes Absent Proteins in Developmental and Pathological Angiogenesis.The American journal of pathology · 2016Article
- Article
- The role of the hypoxia response in shaping retinal vascular development in the absence of Norrin/Frizzled4 signaling.Investigative ophthalmology & visual science · 2014Article
- Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15.Investigative ophthalmology & visual science · 2014Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
purposeTo characterize the features and possible mechanism of plus disease in the mouse oxygen-induced retinopathy (OIR) model for retinopathy of prematurity.
methodsWild-type and Adam (A Disintegrin And Metalloproteinase) knockout mice were exposed to 75% oxygen from postnatal day 7 to 12 (P7 to P12) (hyperoxia), then returned to normal air (relative hypoxia). Live fundus imaging and fluorescein angiography at P17 were compared to immunofluorescence analysis of flat-mounted retinas. Two hallmarks of plus disease, arterial tortuosity and venous dilation, were analyzed on fixed retinas (P12-P17). The length of tortuous vessels was compared to a straight line between two points; the diameter of retinal vessels was determined using ImageJ software, and bromo-deoxyuridine (BrdU) labeling was used to visualize proliferation of retinal vascular cells.
resultsMice developed retinal arterial tortuosity and venous dilation after exposure to OIR, which was visible in live fundus images and fixed whole-mounted retinas. Vein dilation, arterial tortuosity, and BrdU incorporation gradually increased over time. Moreover, Adam8(-/-) and Adam9(-/-) mice and mice lacking Adam10 in endothelial cells were partially protected from plus disease compared to controls.
conclusionsThe mouse OIR model can be used to study the pathogenesis of plus disease and identify potential therapeutic targets. The severity of plus disease increases over time following OIR and correlates with increased proliferation of endothelial cells, suggesting that proliferation of vascular cells may be a mechanism underlying the development of plus disease. Moreover, our findings suggest that ADAMs 8, 9, and 10 could be targets for treatment of plus disease.
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