title: Expression of the adhesion molecules ICAM-1, VCAM-1, and E-selectin and their ligands VLA-4 and LFA-1 in chronic venous leg ulcers.
abstract: BACKGROUND
  Leukocyte binding to endothelial cells (ECs) is thought to contribute to the pathogenesis of leg ulcers caused by chronic venous insufficiency. In other systems, such binding is mediated by the interaction of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule- (VCAM-1) and E-selectin (on ECs), and leukocyte function-associated antigen-1(LFA-1) and very late activated antigen-4 (VLA-4) (on Leukocytes).
  
  
  OBJECTIVE
  Our purpose was to determine whether an increased expression of these adhesion molecules contributes to the pathogenesis of chronic venous insufficiency.
  
  
  METHODS
  Twenty-seven biopsy specimens of inflamed dermatoliposclerotic skin adjacent to venous leg ulcers were stained immunohistochemically with monoclonal antibodies against ICAM-1, VCAM-1, LFA-1, VLA-4, and E-selectin. Staining intensity was compared with that of normal skin.
  
  
  RESULTS
  Specimens of leg ulcers caused by chronic venous insufficiency showed increased expression of ICAM-1 and VCAM-1 but not of E-selectin on The expression of LFA-1 and VLA-4 on perivascular leukocytes was increased dramatically in comparison to healthy skin.
  
  
  CONCLUSIONS
  Upregulation of ICAM-1 and VCAM-1 on ECs may contribute to the increased adherence and extravasation of LFA-1 and VLA-4-positive leukocytes in chronic venous insufficiency.
authors.affiliation: Department of Dermatology, University of Freiburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Weyl
authors.forename: W
authors.initials: W
authors.lastname: Vanscheidt
authors.forename: J M
authors.initials: JM
authors.lastname: Weiss
authors.forename: M
authors.initials: M
authors.lastname: Peschen
authors.forename: E
authors.initials: E
authors.lastname: Schopf
authors.forename: J
authors.initials: J
authors.lastname: Simon
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002448:Cell Adhesion; D002908:Chronic Disease; D019040:E-Selectin / Q000032:analysis / Q000235:genetics*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D039041:Integrin alpha4beta1; D016023:Integrins / Q000032:analysis / Q000235:genetics*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics*; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016201:Receptors, Lymphocyte Homing / Q000032:analysis / Q000235:genetics*; D016029:Receptors, Very Late Antigen / Q000032:analysis / Q000235:genetics*; D012594:Scleroderma, Localized / Q000235:genetics / Q000473:pathology; D012867:Skin / Q000378:metabolism / Q000473:pathology; D013194:Staining and Labeling; D015854:Up-Regulation; D014647:Varicose Ulcer / Q000235:genetics* / Q000473:pathology; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics*; D014689:Venous Insufficiency / Q000235:genetics / Q000473:pathology
chemical_list: D019040:E-Selectin; D039041:Integrin alpha4beta1; D016023:Integrins; D016169:Lymphocyte Function-Associated Antigen-1; D016201:Receptors, Lymphocyte Homing; D016029:Receptors, Very Late Antigen; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1