title: Expression of the PAR-1 protein on the surface of platelets in patients with chronic peripheral arterial insufficiency - preliminary report.
abstract: BACKGROUND
  The activation of pro-coagulation mechanisms associated with the vascular wall's immune and inflammatory responses wall to injury plays a crucial role in the mechanisms of the induction and progression of atherosclerosis.
  
  
  OBJECTIVE
  The aim of this study was to determine the role of protease activated receptors (PAR-1) expressed on the surface of blood platelets in the pathogenesis of chronic peripheral arterial obliterative disease (PAOD) in patients with obliterative atherosclerosis (n = 24) and diabetic macroangiopathy (n = 16), as well as in the controls (n = 12).
  
  
  METHODS
  In addition to the expression of PAR-1, serum/plasma concentrations of thrombin-antithrombin complex (TAT), the von Willebrand factor (vWF), the platelet-derived growth factor, monocyte chemotactic protein, the soluble form of the platelet endothelial cell adhesion molecule, thrombin activatable fibrinolysis inhibitor and interleukin 6 (IL-6) were determined.
  
  
  RESULTS
  Compared to the controls, PAOD patients were characterized by significantly higher levels of PAR-1 expression, vWF, TAT and IL-6. Individuals with diabetic macroangiopathy did not differ significantly from individuals with obliterative atherosclerosis in terms of PAR-1 expression. Upon activation with thrombin receptor antagonist peptide (TRAP), the levels of PAR-1 were comparable in all analyzed groups. In patients with diabetic macroangiopathy, a significant association was observed between the expression of PAR-1 on the surface of the platelet and the serum TAT concentration, as well as between TAT and serum IL-6 concentration.
  
  
  CONCLUSIONS
  Enhanced expression of PAR-1 on the thrombocyte surface in chronic PAOD patients occurs equally in cases of diabetic macroangiopathy and in individuals free from this endocrine pathology.
authors.affiliation: Department and Clinic of Angiology, Hypertension and Diabetology, Wroclaw Medical University, Poland.
authors.forename: Urszula
authors.initials: U
authors.lastname: Jakobsche-Policht
authors.affiliation: Department and Clinic of Angiology, Hypertension and Diabetology, Wroclaw Medical University, Poland.
authors.forename: Dorota
authors.initials: D
authors.lastname: Bednarska-Chabowska
authors.affiliation: Molecular Techniques Unit, Wroclaw Medical University, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Sadakierska-Chudy
authors.affiliation: Department and Clinic of Ophthalmology, Wroclaw Medical University, Poland.
authors.forename: Joanna
authors.initials: J
authors.lastname: Adamiec-Mroczek
mesh_terms: D000990:Antithrombin III; D001792:Blood Platelets / Q000737:chemistry*; D002908:Chronic Disease; D006801:Humans; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D058729:Peripheral Arterial Disease / Q000097:blood*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D044463:Receptor, PAR-1 / Q000097:blood*; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D044463:Receptor, PAR-1; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; D000990:Antithrombin III; D010447:Peptide Hydrolases