Advanced Glycation End Products Modified Protein Up-regulate Adhesion Molecules On Human Endothelial Cell

Objective The infiltration of monocytes/macmphages axuwid P 2-micwglobulin amyloid is one of the moiphologic chamcteiistic of dialysis-related amyloidosis(DRA). Enhanced expression of adhesion molecules on human endothelial cells of syncMal tissue has also been demonstrated in patients ~th dialysis-related amyloidosis. The enhanced expression is in pmportion to the infiltration of monocytes/niacrophages. The study ~s conducted to elucidate the mechanism by which the expression of adhesion molecules on human endothelial cells ~s up-regulatecL Methods Human endothelial cells derived fium umbilical venisQ-IUVEC) were coincubated in viny whh native human sennn albtuiiin(HSA), HSA modified v~ith advanced glycation end products(AGE-HSA) or RPMI-1640 culture medium. The expression of adhesion molecule intereellular adhesion molecule-l(7ICAM-l), vascular cell adhesion molecule-l(VCAM-l) and E-selectin was determined by irnrnunofluorescen staining and flow cytometer analysis. Result ICAM-l and VCAM-l, but not E-selectin ~re constitutively expressed on HUVEC. AGE-HSA enhanced the express of ICAM-l, VCAM-l and E-selectin on HUVEC in a time- and dose- dependent manner. HSA had no effect on the expression of adhesion molecules. Condusion AGE-HSA i~q,-regulates the expression of adhesion molecules on human endothelial cells and therefore promote the infiltration of monocytes4nacmphages wound P 2-micmglobulin amyloid.