Key result
Aminoguanidine at 0.01 mol/l caused an upregulation of ICAM-1 by 48 +/- 17.4% in human umbilical vein endothelial cells, while inhibiting advanced glycation end product formation by 50-57%.
Why the study?
Does aminoguanidine affect the expression of adhesion molecules and AGE formation in human umbilical vein endothelial cells in vitro?
Does aminoguanidine affect the expression of adhesion molecules and AGE formation in human umbilical vein endothelial cells in vitro?
While aminoguanidine inhibits AGE formation, its potential to upregulate ICAM-1 on endothelial cells may hamper its beneficial effects against accelerated atherosclerosis in diabetes.
May offset AGE inhibition benefits in diabetic atherosclerosis; leaves open net endothelial effects pending in vivo data.
The effect of aminoguanidine (AG) on the expression of adhesion molecules on nonactivated human umbilical vein endothelial cells (HUVEC) was investigated in vitro. Nonactivated HUVEC cultivated on long-term glycated fibronectin (FN) as compared to native FN showed a significant upregulation of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and CD31 which could be further promoted by long-term glycated bovine serum albumin. AG, at a concentration of 0.01 mol/l, caused an upregulation of ICAM-1 of 48 +/- 17.4% in HUVEC cultivated on gelatin. In contrast, VCAM-1 and E-selectin remained unaffected. At this concentration, formation of advanced glycation end products (AGE) was inhibited by 57%, as determined immunologically, and by 50%, as verified by AGE-specific fluorescence. A hypothesis concerning the upregulation of ICAM-1 by AG as compared to VCAM-1 is proposed relating to its relative redox insensitivity. Our results demonstrate that the beneficial effect of AG in reducing the risk of accelerated development of atherosclerosis in diabetic patients by inhibiting formation of AGE on matrix proteins such as FN might be hampered by its tendency to upregulate ICAM-1 on endothelial cells.
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Menzel et al. (2008) studied this question. Aminoguanidine was evaluated on Upregulation of ICAM-1. Aminoguanidine at 0.01 mol/l caused an upregulation of ICAM-1 by 48 +/- 17.4% in human umbilical vein endothelial cells, while inhibiting advanced glycation end product formation by 50-57%.
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