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

T. Kunt; T. Forst; O. Harzer; G. Buchert; A. Pfützner; M. Löbig; A. Zschäbitz; E. Stofft; M. Engelbach; J. Beyer

doi:10.1055/s-0029-1211974

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Exp Clin Endocrinol Diabetes 1998; 106(3): 183-188
DOI: 10.1055/s-0029-1211974

Original

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

T. Kunt¹ , T. Forst¹ , O. Harzer¹ , G. Buchert¹ , A. Pfützner¹ , M. Löbig¹ , A. Zschäbitz² , E. Stofft² , M. Engelbach¹ , J. Beyer¹

¹Department of Internal Medicine and Endocrinology, University of Mainz, Germany
²Institute of Anatomy, University of Mainz, Germany

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Publication History

Publication Date:
14 July 2009 (online)

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Summary

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.l) 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 immunoillumino-metric assay (ILMA).

Key words

Advanced glycation endproducts - vascular cell adhesion molecule-1 - intercellular adhesion molecule-1 - E-Selectin

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