Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP.
Medical recordings of 30 patients who received RetCam fluorescein angiography during follow-up and had been treated with anti-VEGF on diagnosis of aggressive posterior ROP in the zone I or zone II between the dates of April 2014-January 2017 were evaluated retrospectively.
The purpose of the present study was to assess the distribution of pericyte/smooth muscle in retinal blood vessels and retinal vasodilator responses in a rat model of ROP.<b>Methods</b>: ROP was induced in rats by the subcutaneous injection of the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8.
Patient characteristics including gestational age, birth weight, gender, stage of ROP at presentation, preoperative treatment (laser, anti-vascular endothelial growth factor (VEGF) or combined), anatomical and functional outcome and complications were recorded.
Astragalus root extract was also found to decrease VEGF and HIF-1α expression, but enhance PEDF and IGF-1 expression in the OIR model mice, thereby protecting retinas in ROP.
Meanwhile, the reduction in angiogenic factors, such as vascular endothelial growth factor (VEGF), can be a protective mechanism for retinopathy of prematurity.
A secondary outcome was the difference in ROP vascular severity score among eyes treated with laser or the vascular endothelial growth factor antagonist bevacizumab.
Intravitreal Delivery of VEGF-A<sub>165</sub>-loaded PLGA Microparticles Reduces Retinal Vaso-Obliteration in an In Vivo Mouse Model of Retinopathy of Prematurity.
The study aimed too ascertain the importance of vascular endothelial growth factor (VEGF), insulin-like growth factor-1 (IGF-1), interleukin-33 (IL-33) and endocan in the diagnosis and follow-up of ROP.
RESULTS The rat model of ROP showed increased serum levels of VEGF, VEGFR-1, and VEGFR-2 compared with the control group, which were decreased in the DAPT group.
Systemic VEGF measurements are important in view of the most appropriate Anti-VEGF drug to be used for the treatment of acute retinopathy of prematurity (ROP).
Ocular neovascularization is a comprehensive process involved in retinal vascular development and several blinding diseases such as age-related macular degeneration and retinopathy of prematurity, with vascular endothelial growth factor (VEGF) regarded as the master regulator.
Oxygen-induced retinopathy (OIR) upregulates Müller cell vascular endothelial growth factor A (VEGFA) that causes intravitreal neovascularization similar to severe retinopathy of prematurity (ROP).
A short-term blockade of the vascular endothelial growth factor (VEGF)-mediated pathway in neonatal rats results in formation of severe retinopathy of prematurity (ROP)-like retinal blood vessels.
Nonselective β-antagonist propranolol is in clinical trials for the treatment of ROP due to its effect of reducing VEGF expression and inhibiting retinal angiogenesis in oxygen-induced ROP models (OIR), but the mechanism by which propranolol acts on ROP vessels is still unclear.
To describe a framework for screening and treatment of retinopathy of prematurity (ROP) using telemedicine screening with laser and/or vascular endothelial growth factor inhibitor treatment strategies.
Using RNA interference for targeted inhibition of VEGF isoforms in conjunction with IGF-I may be preferable for suppression of HREC overgrowth in vasoproliferative retinopathies such as ROP.
Higher VEGF (hazard ratio [HR] = 1.001, P = 0.001) and macrophage inflammatory protein-1β (HR = 1.085, P = 0.022) levels were independently correlated with ROP retreatment.
An OIR mouse model was used to simulate RNV in retinopathy of prematurity (ROP); and the effect of blocking the angiopoietin (Ang) and its receptor (Tie2) and the vascular endothelial growth factor (VEGF) and its receptor (VEGFR) signaling pathways was compared using an IV of sTie2-Fc (Ang inhibitor) and/or ranibizumab (aVEGF antagonist).