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Reversal of Hyperglycemia‐Induced Angiogenesis Deficit of Human Endothelial Cells by Overexpression of Glyoxalase 1 In Vitro
Author(s) -
Ahmed Usman,
Dobler Darin,
Larkin Sarah J.,
Rabbani Naila,
Thornalley Paul J.
Publication year - 2008
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1433.035
Subject(s) - lactoylglutathione lyase , angiogenesis , glycation , methylglyoxal , in vitro , chemistry , endothelial stem cell , medicine , endocrinology , transfection , biochemistry , biology , enzyme , receptor , gene
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.