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Influence of polyclonal antithymocyte globulins on the expression of adhesion molecules of isolated human umbilical vein endothelial cells.

Abstract：

OBJECTIVES:Polyclonal antithymocyte globulins (ATGs) are immunosuppressive agents applied for the treatment and prevention of organ rejection after transplantation. ATGs induce complement-mediated cell death in T lymphocytes and decrease leukocyte adhesion. However, little is known about the effects of ATGs on endothelial cells (EC). Our aim was to study the influence of ATGs upon the expression of adhesion molecules on human umbilical vein endothelial cells (HUVECs) after stimulation with tumor necrosis factor (TNF)-alpha. MATERIAL AND METHODS:HUVECs obtained from umbilical cords were incubated with ATGs before and after 6-hour stimulation with TNF-alpha. The group incubated without ATG served as the controls. Another group was not stimulated with TNF-alpha. By flow cytometry, we analyzed the expression of several adhesion molecules: intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM), platelet EC adhesion molecule (PECAM), and CD62E. Statistical analysis used analysis of variance. RESULTS:After TNF-alpha stimulation, the EC surface expression of ICAM-1 and CD62E was reduced, although not significantly, in treated as compared with untreated cells. The expression of ICAM-1 and CD62E was similar in the unstimulated groups. The expression of VCAM, PECAM, CD55, and CD58 was not modified by ATG treatment. CONCLUSION:Our results demonstrated that ATGs insignificantly reduced the expression of adhesion molecules in HUVECs. The effect of ATGs on stimulated HUVECs remains unclear, probably due to the lack of effector cells.

journal_name

Transplant Proc

journal_title

Transplantation proceedings

authors

Walther S,Beiras-Fernandez A,Csapo C,Münzing S,Stief CG,Hammer C,Reichart B,Thein E

doi

10.1016/j.transproceed.2009.11.038

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

1931-4

issue

5

eissn

0041-1345

issn

1873-2623

pii

S0041-1345(10)00490-2

journal_volume

42

pub_type

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