Curcuminoids inhibit the angiogenic response stimulated by fibroblast growth factor-2, including expression of matrix metalloproteinase gelatinase B

J Biol Chem. 2000 Apr 7;275(14):10405-12. doi: 10.1074/jbc.275.14.10405.

Abstract

We have studied mechanisms controlling activation of the gelatinase B gene (matrix metalloproteinase-9) by fibroblast growth factor-2 (FGF-2) during angiogenesis, and the effects of the natural product curcuminoids on this process. Using a transgenic mouse (line 3445) harboring a gelatinase B promoter/lacZ fusion gene, we demonstrate FGF-2 stimulation of reporter gene expression in endothelial cells of invading neocapillaries in the corneal micropocket assay. Using cultured corneal cells, we show that FGF-2 stimulates DNA binding activity of transcription factor AP-1 but not NF-kappaB and that AP-1 stimulation is inhibited by curcuminoids. We further show that induction of gelatinase B transcriptional promoter activity in response to FGF-2 is dependent on AP-1 but not NF-kappaB response elements and that promoter activity is also inhibited by curcuminoids. In rabbit corneas, the angiogenic response induced by implantation of an FGF-2 pellet is inhibited by the co-implantation of a curcuminoid pellet, and this correlates with inhibition of endogenous gelatinase B expression induced by FGF-2. Angiostatic efficacy in the cornea is also observed when curcuminoids are provided to mice in the diet. Our findings provide evidence that curcuminoids target the FGF-2 angiogenic signaling pathway and inhibit expression of gelatinase B in the angiogenic process.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiogenesis Inhibitors / administration & dosage
  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Cells, Cultured
  • Cornea / blood supply*
  • Curcumin / administration & dosage
  • Curcumin / pharmacology*
  • Diet
  • Female
  • Fibroblast Growth Factor 2 / pharmacology*
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Genes, Reporter
  • Matrix Metalloproteinase 9 / genetics*
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Mice, Transgenic
  • NF-kappa B / metabolism
  • Neovascularization, Pathologic / chemically induced
  • Neovascularization, Pathologic / pathology
  • Neovascularization, Pathologic / prevention & control*
  • Promoter Regions, Genetic
  • Rabbits
  • Recombinant Fusion Proteins / biosynthesis
  • Recombinant Fusion Proteins / genetics
  • Transcription Factor AP-1 / metabolism
  • beta-Galactosidase / genetics

Substances

  • Angiogenesis Inhibitors
  • NF-kappa B
  • Recombinant Fusion Proteins
  • Transcription Factor AP-1
  • Fibroblast Growth Factor 2
  • beta-Galactosidase
  • Matrix Metalloproteinase 9
  • Curcumin