Lipopolysaccharide activates matrix metalloproteinase-2 in endothelial cells through an NF-kappaB-dependent pathway

Biochem Biophys Res Commun. 2000 Mar 16;269(2):401-5. doi: 10.1006/bbrc.2000.2308.

Abstract

Vascular endothelial cells release proteinases that degrade the extracellular matrix, thus enabling cell migration during angiogenesis and vasculogenesis. Endothelial cells secrete mainly the proform of matrix metalloproteinase-2 (proMMP-2). In this report, we examined several growth factors, cytokines, and other molecules for activation of MMP-2 by human umbilical vein endothelial cells. Of these factors, we found that lipopolysaccharide (LPS) is the strongest activator of MMP-2. LPS induced MMP-2 activation in a time- and dose-dependent manner. While pretreatment with zinc chelators or nuclear factor kappaB (NF-kappaB) inhibitors suppressed LPS-induced MMP-2 activation, pretreatment with phosphatidylinositol 3'-kinase inhibitors had no effect. These results indicate that, in endothelial cells, LPS can directly enhance angiogenesis by inducing MMP-2 activation mediated through an NF-kappaB pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / enzymology
  • Enzyme Activation
  • Humans
  • Lipopolysaccharides / pharmacology*
  • Matrix Metalloproteinase 2 / metabolism*
  • NF-kappa B / metabolism
  • Neovascularization, Pathologic
  • Phosphoinositide-3 Kinase Inhibitors

Substances

  • Lipopolysaccharides
  • NF-kappa B
  • Phosphoinositide-3 Kinase Inhibitors
  • Matrix Metalloproteinase 2