The influence of advanced glycation endproducts (AGE) on the expression of human endothelial adhesion molecules

Abstract

Advanced glycation endproducts (AGEs) possibly play a dominant role in the pathogenesis of macrovascular disease in diabetes. Recent studies could demonstrate that glycated albumin (AGE-BSA) was able to stimulate vascular cell adhesion molecule-1 (VCAM.1) on endothelial cells. The aim of this study was to find out if AGE-BSA was not only able to enhance the expression of vascular cell adhesion molecule-1, but also of intercellular adhesion molecule-1 (ICAM-1) and E-Selectin on human endothelial cells. Stimulation of endothelial cells with AGE-BSA for six hours predominantly increased the expression of VCAM-1, but ICAM-1 and E-Selectin were also upregulated as shown by immunoilluminometric assay (ILMA).

Key structural and functional differences between early and advanced glycation products

“…Not only VCAM-1 but also ICAM-1 and E-selectin enhanced expression has been observed after AGE treatment on human endothelial cells (Kunt et al 1998). Even more, AGE activate the function of cell adhesion molecules on lymphoid cells (Kyurkchiev et al 1997).…”

Molecular Effects of C-Peptide in Microvascular Blood Flow Regulation

“…Early features of type 1 diabetes include endothelial dysfunction, increased leukocyte-endothelial adhesion [15], increased blood viscosity [16,17], and changes in the hemodynamic properties of red blood cells [18,19]. All these lead to impaired tissue perfusion, and the development of microvascular complications.…”

Intercellular adhesion molecule‐1 (ICAM‐1) expression is necessary for monocyte adhesion to the placental bed endothelium and is increased in type 1 diabetic human pregnancy

“…AGEs, the end products of non-enzymatic glycosylation of proteins and lipids, are commonly elevated in T1DM, where they are implicated in causing accelerated atheroma [23][24][25]. AGEs are known to stimulate the expression of ICAM-1 expression on endothelial cells.…”