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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2002-4-22
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pubmed:abstractText |
Hypoxia is a potent stimulus to angiogenesis. Expression of the angiogenic growth factor vascular endothelial growth factor (VEGF) and its receptors (VEGFR-1 and VEGFR-2) is up-regulated by hypoxia in a variety of organs and cell lines. We have previously reported that VEGF expression is not increased in renal ischemia-reperfusion injury, although tubular cells concentrate VEGF at their basolateral surface. In this study we assess whether altered VEGF receptor expression compensates for the lack of VEGF regulation during renal ischemia-reperfusion injury.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Endothelial Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vascular Endothelial...,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0085-2538
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
61
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1696-706
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11967019-Animals,
pubmed-meshheading:11967019-Endothelial Growth Factors,
pubmed-meshheading:11967019-Gene Expression,
pubmed-meshheading:11967019-In Situ Hybridization,
pubmed-meshheading:11967019-Kidney,
pubmed-meshheading:11967019-Lymphokines,
pubmed-meshheading:11967019-Male,
pubmed-meshheading:11967019-Neovascularization, Pathologic,
pubmed-meshheading:11967019-Proto-Oncogene Proteins,
pubmed-meshheading:11967019-RNA, Messenger,
pubmed-meshheading:11967019-Rats,
pubmed-meshheading:11967019-Rats, Sprague-Dawley,
pubmed-meshheading:11967019-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:11967019-Receptors, Growth Factor,
pubmed-meshheading:11967019-Receptors, Vascular Endothelial Growth Factor,
pubmed-meshheading:11967019-Reperfusion Injury,
pubmed-meshheading:11967019-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11967019-Vascular Endothelial Growth Factor A,
pubmed-meshheading:11967019-Vascular Endothelial Growth Factor Receptor-1,
pubmed-meshheading:11967019-Vascular Endothelial Growth Factors
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pubmed:year |
2002
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pubmed:articleTitle |
Renal ischemia-reperfusion increases endothelial VEGFR-2 without increasing VEGF or VEGFR-1 expression.
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pubmed:affiliation |
Department of Nephrology, Austin and Repatriation Medical Center, Heidelberg, Victoria, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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