The endothelial receptor tyrosine kinase tie-1 is upregulated by hypoxia and vascular endothelial growth factor

FEBS Lett. 1998 Feb 27;423(3):334-8. doi: 10.1016/s0014-5793(98)00122-7.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta
  • Cattle
  • Cells, Cultured
  • Culture Media, Conditioned / pharmacology
  • Dactinomycin / pharmacology
  • Endothelial Growth Factors / pharmacology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism*
  • Gene Expression Regulation, Developmental / genetics
  • Hypoxia / metabolism*
  • Lymphokines / pharmacology*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Receptor, TIE-1
  • Receptors, Cell Surface / metabolism*
  • Receptors, TIE
  • Transcription, Genetic / genetics
  • Up-Regulation / physiology
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Substances

  • Culture Media, Conditioned
  • Endothelial Growth Factors
  • Lymphokines
  • Receptors, Cell Surface
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Dactinomycin
  • Receptor Protein-Tyrosine Kinases
  • Receptor, TIE-1
  • Receptors, TIE