title: Fibrinolytic activity of endothelial cells from different venous beds.
abstract: BACKGROUND
  Little is known about the molecular biology of endothelial cells from different venous vascular beds. As a result, our treatment of deep vein thrombosis and pulmonary artery embolism remain identical. As an initial step in understanding venous thromboembolic disease in the trauma and surgical patients, this study sought to investigate the balance between coagulation and fibrinolysis in the pulmonary and deep venous vascular beds and how trauma might influence this balance.
  
  
  METHODS
  Confluent human iliac vein endothelial cells (HIVECs) and human pulmonary artery endothelial cells (HPAECs), were cultured in the absence or presence of tumor necrosis factor (TNFα; 10 ng/mL) for 24 h. The expression of mediators of coagulation and fibrinolysis were determined by Western blot analysis, and plasminogen activator activity was determined by a fibrin clot degradation assay.
  
  
  RESULTS
  After TNFα stimulation, there was decreased expression of endothelial protein C receptor and thrombomodulin in both HIVECs and HPAECs. TNFα stimulation increased urokinase plasminogen activator expression in both HIVECs and HPAECs. There was an increase in the expression of tissue plasminogen activator and plasminogen activator inhibitor-1 in response to TNFα in HPAECs, but not in HIVECs. There was significantly greater clot degradation in the presence of both the conditioned media and cell extracts from HIVECs, when compared with HPAECs.
  
  
  CONCLUSIONS
  HPAECs and HIVECs react differently in terms of fibrinolytic potential when challenged with a cytokine associated with inflammation. These findings suggest that endothelial cells from distinct venous vascular beds may differentially regulate the fibrinolytic pathway.
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York.
authors.forename: Neil G
authors.initials: NG
authors.lastname: Kumar
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York.
authors.forename: Amanda
authors.initials: A
authors.lastname: Clark
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York.
authors.forename: Elisa
authors.initials: E
authors.lastname: Roztocil
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York.
authors.forename: Xzabia
authors.initials: X
authors.lastname: Caliste
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York.
authors.forename: David L
authors.initials: DL
authors.lastname: Gillespie
authors.affiliation: Division of Vascular Surgery, Department of Surgery, University of Rochester Medical Center, Rochester, New York. Electronic address: john_cullen@urmc.rochester.edu.
authors.forename: John P
authors.initials: JP
authors.lastname: Cullen
mesh_terms: D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects / Q000502:physiology*; D005342:Fibrinolysis; D006801:Humans; D007084:Iliac Vein / Q000166:cytology* / Q000187:drug effects; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D011651:Pulmonary Artery / Q000166:cytology* / Q000187:drug effects; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D054556:Venous Thromboembolism / Q000097:blood
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D010959:Tissue Plasminogen Activator
keywords: Coagulation; Endothelial cells; Fibrinolysis; TNFα; Vascular beds