Abstract
The receptor tyrosine kinase tie-1 is essential for angiogenesis where it appears to have a role in vessel maturation. Here we have examined the effects of hypoxia and vascular endothelial growth factor (VEGF) on the level of tie-1 protein expressed in bovine aortic endothelial cells. Both hypoxia (2% O2) and VEGF were found to increase tie-1 in a time-dependent manner. Hypoxic induction was direct and effects of hypoxia and VEGF were not additive. Experiments with actinomycin D indicate that these activators regulate tie-1 at the transcriptional level.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aorta
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Cattle
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Cells, Cultured
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Culture Media, Conditioned / pharmacology
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Dactinomycin / pharmacology
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Endothelial Growth Factors / pharmacology*
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / metabolism*
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Gene Expression Regulation, Developmental / genetics
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Hypoxia / metabolism*
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Lymphokines / pharmacology*
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Receptor Protein-Tyrosine Kinases / metabolism*
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Receptor, TIE-1
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Receptors, Cell Surface / metabolism*
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Receptors, TIE
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Transcription, Genetic / genetics
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Up-Regulation / physiology
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
Substances
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Culture Media, Conditioned
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Endothelial Growth Factors
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Lymphokines
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Receptors, Cell Surface
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Dactinomycin
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Receptor Protein-Tyrosine Kinases
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Receptor, TIE-1
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Receptors, TIE