In three murine disease models (the laser-induced choroidal neovascularization model, the VEGF transgenic model, and the retinopathy of prematurity model) significant inhibition of neovascularization (up to 85%) was demonstrated with doses of Ad(GV)PEDF vectors ranging from 1 x 10(8) to 1 x 10(9) pu.
Because ROP is thought to develop under relative hypoxia after exposure to high-dose oxygen, this study was conducted to investigate how estrogen modulates hypoxia-induced VEGF in BRECs and mouse ROP.
Oxygen administration to immature neonates suppresses VEGF-A expression in the retina, resulting in the catastrophic vessel loss that initiates retinopathy of prematurity.
The process of retinal neovascularization in ROP and in animal models of oxygen-induced retinopathy is complex, and involves angiogenic factors, such as vascular endothelial growth factor, and basement membrane components.
VEGF isoforms and their expression after a single episode of hypoxia or repeated fluctuations between hyperoxia and hypoxia: relevance to clinical ROP.
Therefore, the objective of the present study was to determine the effect of local anti-VEGF therapy in a different animal model which closely mimics human ROP.
SB-267268, a nonpeptidic antagonist of alpha(v)beta3 and alpha(v)beta5 integrins, reduces angiogenesis and VEGF expression in a mouse model of retinopathy of prematurity.
Genetic polymorphism may alter the function of the genes which normally control retinal vascularization, such as vascular endothelial growth factor (VEGF), which may also be involved in pathogenesis of ROP.
We used published genetic (i.e., VEGF T(-460)C, G(+ 405)C, and C(-2578)A; IGF-I receptor G(+ 3174)A, angiopoietin II G(-35)C; estrogen receptor PvuII Pp; and endothelial NO-synthase 27-bp b/a and T(-786)C) and birth data of 134 preterm infants without and 103 preterm infants with ROP requiring laser or cryotherapy.
Analysis of: (1) association of VEGF gene polymorphisms and the incidence of ROP, (2) correlation between serum concentration of VEGF and soluble VEGF receptor 1 (sVEGFR-1) during the 1st month of life and the risk of ROP, and (3) correlation between VEGF gene polymorphisms and VEGF serum concentrations.
Vascular endothelial growth factor (VEGF-A) is a major pathogenic factor and a therapeutic target for age-related macular degeneration, diabetic retinopathy, and retinopathy of prematurity.
An accompanying increase in the concentrations of vascular endothelial growth factor and hepatocyte growth factor was found in the peripheral blood of the preterm infants with ROP.
Clinical Relevance Regulation of VEGF may have a role in the development of avascular retina and intravitreous neovascularization in some forms of severe ROP.
Prevention of premature retinopathy by SkQ1 was connected with an increase of VEGF mRNA and protein in OXYS rat's retina up to the levels corresponding to the Wistar rats, and did not involve changes in PEDF expression.