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Journal of Biomedicine and Biotechnology
Volume 2007 (2007), Article ID 41705, 6 pages
Research Article

Expression of VE-Cadherin in Peritubular Endothelial Cells during Acute Rejection after Human Renal Transplantation

1INSERM U331/EA 3740, Faculté de Médecine RTH Laennec, 8 rue Guillaume Paradin, Lyon 69003, France
2Department of Cardiac Transplantation, Hôpital Cardiologique Louis Pradel, 28 avenue du Doyen Lépine, Lyon 69003, France
3Department of Pathology, Hôpital Edouard Herriot, 5 place d'Arsonval, Lyon 69003, France
4Department of Pathology, Hôpital Cardiologique Louis Pradel, 28 avenue du 4 Doyen Lépine, Lyon 69003, France
5Department of Nephrology, Hôpital Edouard Herriot, 5 place d'Arsonval, Lyon 69003, France
6Centre for Cardiovascular Biology & Medicine, King's College London, Strand WC2R 2LS, UK

Received 29 November 2006; Accepted 10 May 2007

Academic Editor: Abdelali Haoudi

Copyright © 2007 Ana Roussoulières et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Genes involved in acute rejection (AR) after organ transplantation remain to be further elucidated. In a previous work we have demonstrated the under-expression of VE-Cadherin by endothelial cells (EC) in AR following murine and human heart transplantation. Serial sections from 15 human kidney Banff-graded transplant biopsies were examined for the presence of VE-Cadherin and CD34 staining by immunohistochemistry (no AR (n=5), AR grade IA (n=5), or AR grade IIA (n=5)). Quantification of peritubular EC staining were evaluated and results were expressed by the percentage of stained cells per surface analysed. There was no difference in CD34 staining between the 3 groups. VE-Cadherin expression was significantly reduced in AR Grade IIA when compared to no AR (P=.01) and to AR grade IA (P=.02). This study demonstrates a reduced VE-Cadherin expression by EC in AR after renal transplantation. The down-regulation of VE-Cadherin may strongly participate in human AR.