The effects of oxygen stresses on the development of features of severe retinopathy of prematurity: knowledge from the 50/10 OIR model

The objective of this study is to determine growth factor expression and activation of signaling pathways associated with intravitreous neovascularization and peripheral avascular retina using a model of retinopathy of prematurity (ROP) relevant to today with oxygen monitoring in neonatal units. Stu...

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Vydané v:Documenta ophthalmologica Ročník 120; číslo 1; s. 25 - 39
Hlavný autor: Elizabeth Hartnett, M.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Berlin/Heidelberg Springer-Verlag 01.02.2010
Springer Nature B.V
Predmet:
Acetophenones - pharmacology
Animals
Disease Models, Animal
Enzyme Inhibitors - pharmacology
Humans
Infant, Newborn
Medicine
Medicine & Public Health
NADPH Oxidases - antagonists & inhibitors
Ophthalmology
Oxidative Stress
Oxygen - toxicity
Rats
Reactive Oxygen Species - antagonists & inhibitors
Reactive Oxygen Species - metabolism
Retinal Neovascularization - etiology
Retinal Neovascularization - metabolism
Retinopathy of Prematurity - etiology
Retinopathy of Prematurity - metabolism
Review Article
Vascular Endothelial Growth Factor A - metabolism
Vitreous Body - blood supply
Oxygen
Retinopathy of prematurity
Intravitreous neovascularization
Vascular endothelial growth factor
NADPH oxidase
50/10 OIR model
ISSN:0012-4486, 1573-2622, 1573-2622
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Shrnutí:The objective of this study is to determine growth factor expression and activation of signaling pathways associated with intravitreous neovascularization and peripheral avascular retina using a model of retinopathy of prematurity (ROP) relevant to today with oxygen monitoring in neonatal units. Studies using 50/10 oxygen-induced retinopathy (OIR) and 50/10 OIR+SO models were reviewed. Repeated fluctuations in oxygen increased retinal vascular endothelial growth factor (VEGF) even while peripheral avascular retina persisted and prior to the development of intravitreous neovascularization. Repeated fluctuations in oxygen increased VEGF 164 expression but not VEGF 120 . Neutralizing VEGF bioactivity significantly reduced intravitreous neovascularization and arteriolar tortuosity without interfering with ongoing retinal vascularization. Repeated oxygen fluctuations led to retinal hypoxia and increased reactive oxygen species (ROS). Inhibiting ROS with NADPH oxidase inhibitor, apocynin, reduced avascular retina by interfering with apoptosis. Supplemental oxygen reduced retinal VEGF concentration and exacerbated NADPH oxidase activation to contribute to intravitreous neovascularization through activation of the JAK/STAT pathway. Oxygen stresses relevant to those experienced by preterm infants today trigger signaling of different pathways to cause avascular retina and intravitreous neovascularization. Increased signaling of VEGF appears important to the development of both avascular retina and intravitreous neovascularization.
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ISSN:0012-4486
1573-2622
1573-2622
DOI:10.1007/s10633-009-9181-x