Reversal of hyperglycemia-induced angiogenesis deficit of human endothelial cells by overexpression of glyoxalase 1 in vitro

Ann N Y Acad Sci. 2008 Apr;1126:262-4. doi: 10.1196/annals.1433.035.


Dicarbonyl glycation of RGD and GFOGER sites in type IV collagen has been associated with decreased angiogenesis. In this study, we investigated whether overexpression of glyoxalase 1 to decrease dicarbonyl glycation would prevent the angiogenesis deficit induced by hyperglycemia in vitro. Transfection of human microvascular endothelial cells resulted in a four-fold increase in glyoxalase 1 activity compared with controls. Incubation of human microvascular endothelial cells in model hyperglycemia produced a 32% decrease in formation of tube structures that was prevented by glyoxalase 1 overexpression. We conclude that increased protection against dicarbonyl glycation of endothelial cell protein protects hyperglycemia-induced angiogenesis deficit.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Endothelium, Vascular / enzymology*
  • Humans
  • Hyperglycemia / complications*
  • Kinetics
  • Lactoylglutathione Lyase / genetics
  • Lactoylglutathione Lyase / metabolism*
  • Microcirculation / drug effects
  • Microcirculation / physiology
  • Neovascularization, Pathologic / etiology*
  • Neovascularization, Pathologic / prevention & control*
  • Transfection


  • Lactoylglutathione Lyase