Tumor necrosis factor-alpha upregulates angiopoietin-2 in human umbilical vein endothelial cells

Biochem Biophys Res Commun. 2000 Mar 16;269(2):361-5. doi: 10.1006/bbrc.2000.2296.

Abstract

The angiopoietin-Tie2 system is an important regulator of vasculogenesis and vascular integrity. Angiopoietin-2 (Ang2) disrupts blood vessel formation in the developing embryo by antagonizing the effects of angiopoietin-1 (Ang1) on the Tie2 receptor. In this study, we examined the effect of a well-known proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), on Ang2 expression in human umbilical vein endothelial cells. Reverse transcriptase-polymerase chain reaction and Northern blot analyses indicated that TNF-alpha induced Ang2 mRNA expression in a time- and dose-dependent manner. Western blot analyses revealed that TNF-alpha treatment increased cellular Ang2 protein. TNF-alpha induced less Ang2 mRNA expression in the presence of nuclear factor-kappaB (NF-kappaB) inhibitor. These results suggest that TNF-alpha-induced inflammatory angiogenesis might be facilitated by the induction of Ang2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiopoietin-2
  • Base Sequence
  • DNA Primers
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Humans
  • NF-kappa B / antagonists & inhibitors
  • Neovascularization, Pathologic / genetics
  • Proteins / genetics*
  • RNA, Messenger / genetics
  • Recombinant Proteins / pharmacology
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Umbilical Veins / cytology
  • Umbilical Veins / drug effects
  • Umbilical Veins / metabolism
  • Up-Regulation / drug effects*

Substances

  • Angiopoietin-2
  • DNA Primers
  • NF-kappa B
  • Proteins
  • RNA, Messenger
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha