Effects of aminoguanidine on adhesion molecule expression of human endothelial cells
| Autor: | Reihsner R, Sengoelge G, Menzel Ej, Neumüller J |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
CD31
Glycation End Products Advanced Intercellular Adhesion Molecule-1 Vascular Cell Adhesion Molecule-1 Guanidines Umbilical vein Rats Sprague-Dawley Tendons Downregulation and upregulation Glycation Animals Humans Cells Cultured Pharmacology Cell adhesion molecule Chemistry Soluble cell adhesion molecules General Medicine Adhesion Molecular biology Biomechanical Phenomena Rats Platelet Endothelial Cell Adhesion Molecule-1 Biochemistry Endothelium Vascular |
| Zdroj: | Pharmacology. 55(3) |
| ISSN: | 0031-7012 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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