Source:http://linkedlifedata.com/resource/pubmed/id/20978476
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001554,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026336,
umls-concept:C0086022,
umls-concept:C0205314,
umls-concept:C0237798,
umls-concept:C0319124,
umls-concept:C0442335,
umls-concept:C0567416,
umls-concept:C0600518,
umls-concept:C0679622,
umls-concept:C0796392,
umls-concept:C1517572,
umls-concept:C1656863,
umls-concept:C1705099
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pubmed:issue |
2
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pubmed:dateCreated |
2011-2-3
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pubmed:abstractText |
Inhibition of vascular endothelial growth factor (VEGF) for the management of the pathological ocular neovascularization associated with diseases such as neovascular age-related macular degeneration is a proven paradigm; however, monthly intravitreal injections are required for optimal treatment. We have previously shown that a novel, secreted anti-VEGF molecule sFLT01 delivered by intravitreal injection of an AAV2 vector (AAV2-sFLT01) gives persistent expression and is efficacious in a murine model of retinal neovascularization. In the present study, we investigate transduction and efficacy of an intravitreally administered AAV2-sFLT01 in a nonhuman primate (NHP) model of choroidal neovascularization (CNV). A dose-dependent and persistent expression of sFLT01 was observed by collecting samples of aqueous humor at different time points over 5 months. The location of transduction as elucidated by in situ hybridization was in the transitional epithelial cells of the pars plana and in retinal ganglion cells. AAV2-sFLT01 was able to effectively inhibit laser-induced CNV in a dose-dependent manner as determined by comparing the number of leaking CNV lesions in the treated versus control eyes using fluorescein angiography. Our data suggest that intravitreal delivery of AAV2-sFLT01 may be an effective long-term treatment for diseases caused by ocular neovascularization.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1525-0024
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pubmed:author |
pubmed-author:CollinsMargaretM,
pubmed-author:DuFresneElizabethE,
pubmed-author:FlaxelChristinaC,
pubmed-author:HauswirthWilliamW,
pubmed-author:KimIvanaI,
pubmed-author:KissSzilardS,
pubmed-author:LiQiuhongQ,
pubmed-author:LukasonMichaelM,
pubmed-author:MaclachlanTimothyT,
pubmed-author:MillerJoanJ,
pubmed-author:PechanPeterP,
pubmed-author:RubinHillardH,
pubmed-author:ScariaAbrahamA,
pubmed-author:WadsworthSamuelS
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pubmed:issnType |
Electronic
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
260-5
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pubmed:meshHeading |
pubmed-meshheading:20978476-Animals,
pubmed-meshheading:20978476-Choroidal Neovascularization,
pubmed-meshheading:20978476-Dependovirus,
pubmed-meshheading:20978476-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:20978476-Genetic Vectors,
pubmed-meshheading:20978476-In Situ Hybridization,
pubmed-meshheading:20978476-Intravitreal Injections,
pubmed-meshheading:20978476-Macaca fascicularis,
pubmed-meshheading:20978476-Mice,
pubmed-meshheading:20978476-Mice, Inbred C57BL,
pubmed-meshheading:20978476-Vascular Endothelial Growth Factor A,
pubmed-meshheading:20978476-Vascular Endothelial Growth Factor Receptor-1
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pubmed:year |
2011
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pubmed:articleTitle |
Inhibition of choroidal neovascularization in a nonhuman primate model by intravitreal administration of an AAV2 vector expressing a novel anti-VEGF molecule.
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pubmed:affiliation |
Genzyme Corporation, Framingham, MA, USA.
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pubmed:publicationType |
Journal Article
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