title: Significance of vitronectin and PAI-1 activity levels in carotid artery disease: comparison of symptomatic and asymptomatic patients.
abstract: OBJECTIVE
  Carotid atherosclerosis one of the main risk factors for ischemic stroke. Acute thrombosis after atherosclerotic plaque disruption is a major complication of primary atherosclerosis, leading to acute ischemic syndromes and atherosclerotic progression. PAI-1 is the most important and most rapidly acting physiological inhibitor of tissue-type (t-PA) and urokinase type (u-PA) plasminogen activators. Active PAI-1 form spontaneously converts to the latent with a half-life of ~1 h. Complex formation with vitronectin increases half life of PAI-1 by two- to four-folds. Thus, this inhibitor function of PAI-1 facilitated by Vn that binds the inhibitor and may regulate its activity by the stabilizing the active PAI-1 conformation. In addition, PAI-1/VN complexes may effect vascular structure and function. However, the exact role of these complexes in vascular remodelling are not completely clear. The aim of the present study was determining, correlating and comparing the plasma vitronectin, t-PA and PAI-1 activity levels in asymptomatic and symptomatic patients with carotid artery plaque.
  
  
  METHODS
  A total of 37 carotid artery disease patients were included in this study. Blood samples were obtained from Cerrahpasa Medical School, Department of Heart and Vessel Surgery, University of Istanbul. Plasma vitronectin, tPA and PAI-1 activity levels were determined by ELISA.
  
  
  RESULTS
  We found plasma PAI-1 activity levels were elevated in the asymptomatic group as compared with symptomatic group (P=0.038). We have also found a positive correlation between PAI-1 activity and vitronectin levels in symptomatic group (r=0.399, P=0.039).
  
  
  CONCLUSIONS
  Decreased PAI-1 activity levels correlate with vitronectin in the symptomatic group; a) may be the consequence a compensatory mechanisms (due to possibilty in increased fibrinolytic activity and decreased vascular remodelling) against disease progression. b) or may be also cause progression of disease by increase of vascular remodelling.
authors.affiliation: Department of Biochemistry, Cerrahpasa Medical School, University of Istanbul, Istanbul, Turkey. ozlembal2000@yahoo.com
authors.forename: H
authors.initials: H
authors.lastname: Ekmekçi
authors.forename: Z
authors.initials: Z
authors.lastname: Güngör Öztürk
authors.forename: O B
authors.initials: OB
authors.lastname: Ekmekçi
authors.forename: I
authors.initials: I
authors.lastname: Işler Bütün
authors.forename: K
authors.initials: K
authors.lastname: Beşirli
authors.forename: S
authors.initials: S
authors.lastname: Gode
authors.forename: P
authors.initials: P
authors.lastname: Atukeren
authors.forename: H
authors.initials: H
authors.lastname: Sönmez
mesh_terms: D000368:Aged; D058070:Asymptomatic Diseases; D015415:Biomarkers / Q000097:blood; D016893:Carotid Stenosis / Q000097:blood* / Q000150:complications; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D014568:Urokinase-Type Plasminogen Activator / Q000097:blood*; D019096:Vitronectin / Q000097:blood*
chemical_list: D015415:Biomarkers; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; D019096:Vitronectin; D014568:Urokinase-Type Plasminogen Activator