Linked Life Data

12652651

Source:http://linkedlifedata.com/resource/pubmed/id/12652651

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-3-24
pubmed:abstractText
Vascular endothelial growth factor (VEGF) plays a central role in the development of retinal neovascularization and diabetic macular edema. There is also evidence suggesting that VEGF is an important stimulator for choroidal neovascularization. In this study, we investigated the effect of a specific inhibitor of VEGF, VEGF-TRAP(R1R2), in models for these disease processes. VEGF-TRAP(R1R2) is a fusion protein, which combines ligand binding elements taken from the extracellular domains of VEGF receptors 1 and 2 fused to the Fc portion of IgG1. Subcutaneous injections or a single intravitreous injection of VEGF-TRAP(R1R2) strongly suppressed choroidal neovascularization in mice with laser-induced rupture of Bruch's membrane. Subcutaneous injection of VEGF-TRAP(R1R2) also significantly inhibited subretinal neovascularization in transgenic mice that express VEGF in photoreceptors. In two models of VEGF-induced breakdown of the blood-retinal barrier (BRB), one in which recombinant VEGF is injected into the vitreous cavity and one in which VEGF expression is induced in the retina in transgenic mice, VEGF-TRAP(R1R2) significantly reduced breakdown of the BRB. These data confirm that VEGF is a critical stimulus for the development of choroidal neovascularization and indicate that VEGF-TRAP(R1R2) may provide a new agent for consideration for treatment of patients with choroidal neovascularization and diabetic macular edema.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
195
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-8
pubmed:dateRevised
2011-7-26
pubmed:meshHeading
pubmed-meshheading:12652651-Animals, pubmed-meshheading:12652651-Blood-Retinal Barrier, pubmed-meshheading:12652651-Choroid, pubmed-meshheading:12652651-Choroid Diseases, pubmed-meshheading:12652651-Diabetic Retinopathy, pubmed-meshheading:12652651-Disease Models, Animal, pubmed-meshheading:12652651-Endothelial Growth Factors, pubmed-meshheading:12652651-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12652651-Lymphokines, pubmed-meshheading:12652651-Mice, pubmed-meshheading:12652651-Mice, Inbred C57BL, pubmed-meshheading:12652651-Mice, Transgenic, pubmed-meshheading:12652651-Neovascularization, Pathologic, pubmed-meshheading:12652651-Receptors, Growth Factor, pubmed-meshheading:12652651-Recombinant Fusion Proteins, pubmed-meshheading:12652651-Retina, pubmed-meshheading:12652651-Retinal Artery, pubmed-meshheading:12652651-Vascular Endothelial Growth Factor A, pubmed-meshheading:12652651-Vascular Endothelial Growth Factors
pubmed:year
2003
pubmed:articleTitle
VEGF-TRAP(R1R2) suppresses choroidal neovascularization and VEGF-induced breakdown of the blood-retinal barrier.
pubmed:affiliation
The Department of Ophthalmology, The Johns Hopkins University School of Medicine, Maumenee, Baltimore, Maryland, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't