ArticleInvestigative ophthalmology & visual science2014
Mitigation of oxygen-induced retinopathy in α2β1 integrin-deficient mice.
Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Single-Molecule Imaging of Membrane Proteins on Vascular Endothelial Cells.Journal of lipid and atherosclerosis · 2023Review
- Article
- Irisin Attenuates Pathological Neovascularization in Oxygen-Induced Retinopathy Mice.Investigative ophthalmology & visual science · 2022Article
- Inhibitory effect of maspinon neovascularization in diabetic retinopathy.World journal of diabetes · 2021Article
- Review
- Gpr116 Receptor Regulates Distinctive Functions in Pneumocytes and Vascular Endothelium.PloS one · 2015Article
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Authors and funding
8 authors.
Funding
Abstract
purposeThe α2β1 integrin plays an important but complex role in angiogenesis and vasculopathies. Published GWAS studies established a correlation between genetic polymorphisms of the α2β1 integrin gene and incidence of diabetic retinopathy. Recent studies indicated that α2-null mice demonstrate superior vascularization in both the wound and diabetic microenvironments. The goal of this study was to determine whether the vasculoprotective effects of α2-integrin deficiency extended to the retina, using the oxygen-induced retinopathy (OIR) model for retinopathy of prematurity (ROP).
methodsIn the OIR model, wild-type (WT) and α2-null mice were exposed to 75% oxygen for 5 days (postnatal day [P] 7 to P12) and subsequently returned to room air for 6 days (P12-P18). Retinas were collected at postnatal day 7, day 13, and day 18 and examined via hematoxylin and eosin and Lectin staining. Retinas were analyzed for retinal vascular area, neovascularization, VEGF expression, and Müller cell activation. Primary Müller cell cultures from WT and α2-null mice were isolated and analyzed for hypoxia-induced VEGF-A expression.
resultsIn the retina, the α2β1 integrin was minimally expressed in endothelial cells and strongly expressed in activated Müller cells. Isolated α2-null primary Müller cells demonstrated decreased hypoxia-induced VEGF-A expression. In the OIR model, α2-null mice displayed reduced hyperoxia-induced vaso-attenuation, reduced pathological retinal neovascularization, and decreased VEGF expression as compared to WT counterparts.
conclusionsOur data suggest that the α2β1 integrin contributes to the pathogenesis of retinopathy. We describe a newly identified role for α2β1 integrin in mediating hypoxia-induced Müller cell VEGF-A production.
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