title: Influence of polyclonal antithymocyte globulins on the expression of adhesion molecules of isolated human umbilical vein endothelial cells.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiac Surgery, LM University Hospital, Munich, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Walther
authors.forename: A
authors.initials: A
authors.lastname: Beiras-Fernandez
authors.forename: C
authors.initials: C
authors.lastname: Csapo
authors.forename: S
authors.initials: S
authors.lastname: Münzing
authors.forename: C G
authors.initials: CG
authors.lastname: Stief
authors.forename: C
authors.initials: C
authors.lastname: Hammer
authors.forename: B
authors.initials: B
authors.lastname: Reichart
authors.forename: E
authors.initials: E
authors.lastname: Thein
mesh_terms: D000961:Antilymphocyte Serum / Q000494:pharmacology*; D015815:Cell Adhesion Molecules / Q000302:isolation & purification / Q000378:metabolism*; D019040:E-Selectin / Q000235:genetics; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005434:Flow Cytometry; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014470:Umbilical Cord; D014471:Umbilical Veins / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics
chemical_list: D000961:Antilymphocyte Serum; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1