title: Human pulmonary valve endothelial cells express functional adhesion molecules for leukocytes.
abstract: OBJECTIVE
  Histopathological studies of rejected orthotopic heart transplants suggest that cardiac valve endothelium is spared the inflammatory cell infiltration and tissue damage that occurs in the myocardium. To test whether this apparent protection from leukocyte invasion might be an inherent feature of the valve endothelium, leukocyte adhesion molecule expression and function were analyzed in human pulmonary valve endothelial cells (HPVEC). Use of cultured HPVEC allowed delineation of the potential contribution of functional adhesion molecules from the contribution of hemodynamic forces exerted on the leaflet surface in vivo
  
  
  RESULTS
  HPVEC express E-selectin, ICAM-1, and VCAM-1 in response to the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) similarly to other types of cultured human endothelial cells. In a static cell adhesion assay, E-selectin-mediated adhesion of HL-60 cells, a human promyelocytic leukemia cell line, and U937 cells, a human monocytic cell line, was determined in cells treated with TNF-alpha for 5 h. After 24 h of TNF-alpha, adhesion of U937 cells to HPVEC was mediated primarily by VCAM-1, consistent with the high expression of VCAM-1 and diminished expression of E-selectin at 24 h.
  
  
  CONCLUSIONS
  These results demonstrate that HPVEC express functional leukocyte adhesion molecules in vitro and suggest that cardiac valve endothelium is competent to initiate leukocyte adhesion. Thus, other factors, such as the hemodynamic forces exerted on the valve, may contribute to the apparent protection from inflammatory cell infiltration in vivo.
authors.affiliation: Department of Surgery, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA.
authors.forename: Evan L
authors.initials: EL
authors.lastname: Dvorin
authors.forename: Joel
authors.initials: J
authors.lastname: Jacobson
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Roth
authors.forename: Joyce
authors.initials: J
authors.lastname: Bischoff
mesh_terms: D000293:Adolescent; D000328:Adult; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001900:Boston; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000187:drug effects / Q000502:physiology*; D002648:Child; D002669:Child Welfare; D002675:Child, Preschool; D016207:Cytokines / Q000096:biosynthesis / Q000187:drug effects; D019040:E-Selectin / Q000096:biosynthesis / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000502:physiology*; D005434:Flow Cytometry; D006084:Graft Rejection / Q000378:metabolism / Q000503:physiopathology; D018922:HL-60 Cells / Q000187:drug effects / Q000502:physiology; D016027:Heart Transplantation; D006801:Humans; D007223:Infant; D007229:Infant Welfare; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000187:drug effects; D019007:P-Selectin / Q000096:biosynthesis / Q000187:drug effects; D011664:Pulmonary Valve / Q000166:cytology*; D012867:Skin / Q000166:cytology; D017211:Treatment Failure; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000187:drug effects; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D015815:Cell Adhesion Molecules; D016207:Cytokines; D019040:E-Selectin; D019007:P-Selectin; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1