title: Aspirin inhibits endothelial cell activation induced by antiphospholipid antibodies.
abstract: BACKGROUND
  Antiphospholipid antibodies (APLA) have been shown to activate endothelial cells (EC) in vitro, as documented by an increased expression of tissue factor as well as leukocyte adhesion molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin. Currently, treatment of patients with the antiphospholipid syndrome includes aspirin, particularly for women with recurrent fetal loss.
  
  
  OBJECTIVE
  The present study was undertaken to investigate whether aspirin interferes with EC activation induced by APLA in vitro.
  
  
  METHODS
  IgG from 14 patients with APLA, and suffering from thrombotic complications and/or pregnancy morbidity, and control IgG were tested for their ability to modify the expression of VCAM-1 in human umbilical vein endothelial cells. VCAM-1 antigen was measured by flow cytometry and its mRNA by quantitative reverse transcriptase-polymerase chain reaction.
  
  
  RESULTS
  Incubation of EC with IgG from most of the patients led to a higher VCAM-1 expression compared with incubation with control IgG. The effect of aspirin was studied for the eight IgG samples that induced a more than 50% increase in VCAM-1. Aspirin (10 mm) treatment of the cells significantly reduced the VCAM-1 response to these APLA.
  
  
  CONCLUSIONS
  Our results indicate that besides its antiplatelet properties, aspirin exerts a protective effect towards APLA at the EC level by decreasing leukocyte adhesion molecule expression at the cell surface.
authors.affiliation: Division of Angiology and Hemostasis, University Hospital, Geneva, Switzerland.
authors.forename: S
authors.initials: S
authors.lastname: Dunoyer-Geindre
authors.forename: E K O
authors.initials: EK
authors.lastname: Kruithof
authors.forename: F
authors.initials: F
authors.lastname: Boehlen
authors.forename: N
authors.initials: N
authors.lastname: Satta-Poschung
authors.forename: G
authors.initials: G
authors.lastname: Reber
authors.forename: P
authors.initials: P
authors.lastname: de Moerloose
mesh_terms: D017152:Antibodies, Antiphospholipid / Q000494:pharmacology*; D016736:Antiphospholipid Syndrome / Q000473:pathology; D001241:Aspirin / Q000494:pharmacology*; D016022:Case-Control Studies; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology; D014471:Umbilical Veins / Q000166:cytology; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics
chemical_list: D017152:Antibodies, Antiphospholipid; D007074:Immunoglobulin G; D019010:Vascular Cell Adhesion Molecule-1; D001241:Aspirin