Source:http://linkedlifedata.com/resource/pubmed/id/18027100
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2008-4-22
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| pubmed:abstractText |
The genes that regulate the formation of blood vessels in adult tissues represent promising therapeutic targets because angiogenesis plays a role in many diseases, including cancer. We wished to develop a mouse model allowing characterization of gene function in adult angiogenic vasculature while minimizing effects on embryonic vasculature or adult quiescent vasculature. Here we describe a transgenic mouse model that allows expression of proteins in the endothelial cells of newly forming blood vessels in the adult using a selective retroviral gene delivery system. We generated transgenic mouse lines that express the TVA receptor for the RCAS avian-specific retrovirus from Flk1 gene regulatory elements that drive expression in proliferating endothelial cells. Several of these Flk1-TVA lines expressed TVA mRNA in the embryonic vasculature and TVA protein in new blood vessels growing into subcutaneous extracellular matrix implants in adult mice. In a Flk1-TVA line that was crossed with the MMTV-PyMT transgenic mammary tumor model, tumor endothelial cells also expressed the TVA protein. Furthermore, endothelial cells in extracellular matrix implants and the tumors of Flk1-TVA mice were susceptible to RCAS infection, as determined by expression of green fluorescent protein encoded by the virus. The Flk1-TVA mouse model in conjunction with the RCAS gene delivery system will be useful to study molecular mechanisms underlying adult forms of angiogenesis.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0962-8819
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
17
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
403-15
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:18027100-Alpharetrovirus,
pubmed-meshheading:18027100-Animals,
pubmed-meshheading:18027100-Avian Proteins,
pubmed-meshheading:18027100-Blood Vessels,
pubmed-meshheading:18027100-Cells, Cultured,
pubmed-meshheading:18027100-Cloning, Molecular,
pubmed-meshheading:18027100-Disease Susceptibility,
pubmed-meshheading:18027100-Embryo, Mammalian,
pubmed-meshheading:18027100-Female,
pubmed-meshheading:18027100-Gene Expression Regulation, Developmental,
pubmed-meshheading:18027100-Gene Transfer Techniques,
pubmed-meshheading:18027100-Humans,
pubmed-meshheading:18027100-Mice,
pubmed-meshheading:18027100-Mice, Transgenic,
pubmed-meshheading:18027100-Models, Biological,
pubmed-meshheading:18027100-Neovascularization, Physiologic,
pubmed-meshheading:18027100-Receptors, Virus,
pubmed-meshheading:18027100-Retroviridae Infections,
pubmed-meshheading:18027100-Terminal Repeat Sequences,
pubmed-meshheading:18027100-Transgenes,
pubmed-meshheading:18027100-Vascular Endothelial Growth Factor Receptor-2
|
| pubmed:year |
2008
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| pubmed:articleTitle |
A novel Flk1-TVA transgenic mouse model for gene delivery to angiogenic vasculature.
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| pubmed:affiliation |
Burnham Institute for Medical Research, 10901 N. Torrey Pines Rd., La Jolla, CA 92037, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
|