Anti-angiogenic properties of a sulindac analogue

Br J Pharmacol. 2007 Dec;152(8):1207-14. doi: 10.1038/sj.bjp.0707534. Epub 2007 Oct 29.

Abstract

Background and purpose: Angiopoietins (Ang) are crucial for new blood vessel formation and exert their effects by acting on the Tie2 receptor. We have recently described a sulindac analogue 2-((1E,Z)-1-benzylidene-5-bromo-2-methyl-1H-inden-3-yl)acetic acid; termed C-18 from now onwards) that inhibits Tie2 receptor activity in kinase assays in vitro. Here, we have assessed the ability of C-18 to inhibit angiogenesis-related properties of endothelial cells and tested its selectivity for the Tie2 receptor.

Experimental approach: For in vitro experiments human umbilical vein endothelial cells (HUVEC) were used. Proliferation was measured using the MTT assay; migration assays were performed in a modified Boyden chamber and tube-like structure formation was determined on matrigel. The effects of C-18 in vivo were evaluated in the chicken chorioallantoic membrane (CAM).

Key results: Pre-treatment of HUVEC with C-18 blocked Ang-1-stimulated migration, but also abolished vascular endothelial cell growth factor (VEGF)- and fibroblast growth factor 2-induced responses. Incubation with C-18 inhibited serum-induced proliferation in a concentration-dependent manner; C-18 was, however, without effect on Ang-1-induced survival. In addition, we observed that C-18 did not inhibit ligand-induced receptor phosphorylation of Tie2 or VEGFR2. On the other hand, C-18 blocked activation of members of the mitogen-activated protein kinase family and of the Ser/Thr kinase Akt induced by both VEGF and Ang-1. Furthermore, incubation of CAMs with C-18 led to a dose-dependent inhibition of vascular length.

Conclusions and implications: C-18 did not act as a Tie2 inhibitor, as originally thought, but rather inhibited growth factor-stimulated signalling pathways that regulate endothelial cell migration and potently reduces neovascularization in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Angiopoietin-1 / antagonists & inhibitors
  • Animals
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Chick Embryo
  • Chorioallantoic Membrane / drug effects
  • Chorioallantoic Membrane / metabolism
  • Dose-Response Relationship, Drug
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Fibroblast Growth Factor 2 / drug effects
  • Fibroblast Growth Factor 2 / metabolism
  • Humans
  • Mitogen-Activated Protein Kinases / drug effects
  • Mitogen-Activated Protein Kinases / metabolism
  • Phosphorylation / drug effects
  • Protein Serine-Threonine Kinases / drug effects
  • Protein Serine-Threonine Kinases / metabolism
  • Receptor, TIE-2 / drug effects*
  • Receptor, TIE-2 / metabolism
  • Signal Transduction / drug effects
  • Sulindac / administration & dosage
  • Sulindac / pharmacology
  • Umbilical Veins
  • Vascular Endothelial Growth Factor A / drug effects
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • 2-(1-benzylidene-5-bromo-2-methyl-1H-inden-3-yl)acetic acid
  • Angiogenesis Inhibitors
  • Angiopoietin-1
  • Vascular Endothelial Growth Factor A
  • Fibroblast Growth Factor 2
  • Sulindac
  • Receptor, TIE-2
  • Protein Serine-Threonine Kinases
  • Mitogen-Activated Protein Kinases