title: Expression of fibrinolytic antigens in redistributed cardiac mast cells in auricular thrombosis.
abstract: Recent data suggest that auricular thrombosis is associated with an increase and accumulation of mast cells (MC) in the subendothelial region of the upper endocardium. However, the molecular basis and the functional role of MC in this process are not known. In the current study, expression of fibrinolytic and antifibrinolytic antigens in human cardiac MC was analyzed by immunohistochemistry. MC were found to react with antibodies against tissue-type plasminogen activator (tPA) and urokinase receptor (uPAR/CD87), but not with antibodies against urokinase (uPA) or plasminogen activator inhibitors (PAI-1, PAI-2). Significant changes were observed when the phenotype of accumulated MC in the upper endocardium in patients with auricular thrombosis was compared with the phenotype of myocardial MC in the same patients or with MC in normal hearts. These redistributed MC stained less intensely with antibodies against tPA and chymase but retained their staining for tryptase and uPAR. Together, these data indicate that cardiac MC are a source of fibrinolytic antigens and that accumulation of MC in auricular thrombosis is associated with phenotypic changes of MC and loss of cellular tPA. It is hypothesized that MC and their products may play a role in endogenous fibrinolysis in auricular thrombosis.
authors.affiliation: Department of Internal Medicine I, University of Vienna, Austria.
authors.forename: H C
authors.initials: HC
authors.lastname: Bankl
authors.forename: T
authors.initials: T
authors.lastname: Radaszkiewicz
authors.forename: B
authors.initials: B
authors.lastname: Pikula
authors.forename: M
authors.initials: M
authors.lastname: Baghestanian
authors.forename: M R
authors.initials: MR
authors.lastname: Mehrabi
authors.forename: H
authors.initials: H
authors.lastname: Bankl
authors.forename: K
authors.initials: K
authors.lastname: Lechner
authors.forename: P
authors.initials: P
authors.lastname: Valent
mesh_terms: D000933:Antifibrinolytic Agents / Q000378:metabolism; D002478:Cells, Cultured; D053818:Chymases; D004699:Endocardium / Q000378:metabolism; D005343:Fibrinolytic Agents / Q000378:metabolism*; D006325:Heart Atria / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D006493:Heparin / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008407:Mast Cells / Q000378:metabolism*; D008934:Mitogens / Q000378:metabolism; D009206:Myocardium / Q000276:immunology / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D010960:Plasminogen Activators / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism; D018121:Receptors, Cytokine / Q000378:metabolism; D055293:Receptors, Urokinase Plasminogen Activator; D012697:Serine Endopeptidases / Q000378:metabolism; D019089:Stem Cell Factor / Q000378:metabolism / Q000494:pharmacology; D013927:Thrombosis; D010959:Tissue Plasminogen Activator / Q000378:metabolism; D053802:Tryptases; D014568:Urokinase-Type Plasminogen Activator / Q000378:metabolism
chemical_list: D000933:Antifibrinolytic Agents; D005343:Fibrinolytic Agents; D008934:Mitogens; C524898:PLAUR protein, human; D017395:Plasminogen Activator Inhibitor 1; D011956:Receptors, Cell Surface; D018121:Receptors, Cytokine; D055293:Receptors, Urokinase Plasminogen Activator; D019089:Stem Cell Factor; D006493:Heparin; D010960:Plasminogen Activators; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator