Abstract
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.
Highlights
Acute rejection, observed after renal transplantation, has a significant impact for long-term renal allograft survival
In a previous work [14] we have demonstrated that VE-Cadherin is under expressed in acute rejection in a murine heterotopic heart transplantation model and in acute rejection following human heart transplantation
We demonstrate that VE-Cadherin is under expressed in acute rejection after renal transplantation
Summary
Acute rejection, observed after renal transplantation, has a significant impact for long-term renal allograft survival. Released cytokines target vascular endothelial cells, the first cells to be recognized by the host’s immune system, and induce the expression of adhesion molecules and chemokines implicated in T-lymphocyte adhesion and extravasation. Initial transient adhesion of Tlymphocytes mediated principally by selectins induce the rolling of the T-cells and their subsequent activation and adhesion on the endothelium via other adhesion molecules such as ICAM-1 and VCAM-1. Endothelial cells coating the capillaries that act as a barrier between the donor organ and recipient bears the MHC class II molecules. They are highly responsive to cytokines and express adhesion and other molecules implicated in T-lymphocyte adhesion and extravasation. We demonstrate that VE-Cadherin is under expressed in acute rejection after renal transplantation
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