Receptors for advanced glycation end-products (AGE) - Expression by endothelial cells in non-diabetic uraemic patients

被引:39
作者
Greten, J
Kreis, I
Wiesel, K
Stier, E
Schmidt, AM
Stern, DM
Ritz, E
Waldherr, R
Nawroth, PP
机构
[1] UNIV HEIDELBERG,DEPT SURG,W-6900 HEIDELBERG,GERMANY
[2] UNIV HEIDELBERG,DEPT PATHOL,W-6900 HEIDELBERG,GERMANY
[3] COLUMBIA UNIV,NEW YORK,NY
[4] COLL PHYS & SURG,NEW YORK,NY
关键词
D O I
10.1093/oxfordjournals.ndt.a027399
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
Background. Cellular actions of advanced glycation end-products (AGE) are mediated by a receptor for AGE (RAGE), a novel integral membrane protein. Immunohistochemical studies show only low-level RAGE antigen expression in endothelial cells. Design. It was the purpose of the study to compare expression of RAGE antigen by endothelial cells in non-diabetic uraemic patients (n = 8) with non-uraemic controls (n = 11). Samples of arterial tissue were obtained at the time of renal transplantation (in uraemic patients) and abdominal surgery (in controls). RAGE antigen was visualized using guinea-pig anti-RAGE IgG and PAP technique. Results. Marked staining for RAGE was noted in endothelial cells, both arterial endothelium and endothelium of vasa vasorum of normoglycaemic uraemic patients, but was not demonstrable in endothelial cells of large arteries and only faintly expressed in vasa vasorum of non-uraemic individuals. Conclusion. Normal endothelial cells do not constitually express RAGE antigen, in contrast it is expressed by arterial and capillary endothelial cells of uraemic patients. The observation is of note in view of the putative role of AGE of causing atherosclerotic and non-atherosclerotic vascular lesions.
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页码:786 / 790
页数:5
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