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晚期糖基化终产物(AGE)受体——非糖尿病尿毒症患者内皮细胞的表达

Receptors for advance glycation end-products (AGE) - expression by endothelial cells in non-diabetic uraemic patients.

作者信息

Greten J, Kreis I, Wiesel K, Stier E, Schmidt A M, Stern D M, Ritz E, Waldherr R, Nawroth P P

机构信息

Department of Medicine, University of Heidelberg, Germany.

出版信息

Nephrol Dial Transplant. 1996 May;11(5):786-90. doi: 10.1093/oxfordjournals.ndt.a027399.

DOI:10.1093/oxfordjournals.ndt.a027399
PMID:8671895
Abstract

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 purposes 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.

摘要

背景

晚期糖基化终产物(AGE)的细胞作用是由一种新型整合膜蛋白——AGE受体(RAGE)介导的。免疫组织化学研究显示,内皮细胞中仅存在低水平的RAGE抗原表达。设计:本研究旨在比较非糖尿病尿毒症患者(n = 8)与非尿毒症对照者(n = 11)内皮细胞中RAGE抗原的表达情况。在肾移植时(尿毒症患者)和腹部手术时(对照者)获取动脉组织样本。使用豚鼠抗RAGE IgG和PAP技术使RAGE抗原可视化。

结果

在血糖正常的尿毒症患者的内皮细胞中,包括动脉内皮和滋养血管内皮,均观察到RAGE的明显染色,但在大动脉内皮细胞中未检测到,在非尿毒症个体的滋养血管中仅微弱表达。

结论

正常内皮细胞不组成性表达RAGE抗原;相反,尿毒症患者的动脉和毛细血管内皮细胞表达该抗原。鉴于AGE在引起动脉粥样硬化和非动脉粥样硬化性血管病变中的假定作用,这一观察结果值得关注。

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