title: Course of platelet activation markers after ischemic stroke.
abstract: OBJECTIVE
  The aim of this study was to evaluate the time course of platelet activation after ischemic stroke and to investigate whether platelet activation and inflammation are correlated with each other.
  
  
  METHODS
  We serially determined expression of p-selectin (CD62p) and lysosome-associated membrane protein (CD63) by platelets using flow cytometry at 10 time points between days 1 and 90 in patients after ischemic stroke (n=50), in healthy subjects (n=30), and in risk factor control subjects (n=20). Furthermore, we correlated leukocyte count, C-reactive protein, and fibrinogen levels with platelet activation markers.
  
  
  RESULTS
  CD62p and CD63 expression was higher on day 1 after stroke than in both control groups (P<0.005 for both). CD62p expression rapidly declined, whereas CD63 expression remained significantly elevated until day 90. Stroke severity and different medication for secondary stroke prevention did not influence CD62p or CD63 expression. Platelet activation markers and inflammatory parameters were not correlated with each other at any time point after stroke.
  
  
  CONCLUSIONS
  The initial increase in both CD62p and CD63 expression by platelets is followed by a differential regulation of both parameters after stroke. The rapid decrease in CD62p expression may be caused by shedding from the cell surface. Its persistent elevation makes CD63 a good candidate for studies on predictors for stroke recurrence. Our findings suggest that the expression of CD62p and CD63 by platelets is regulated independently from inflammatory indexes.
authors.affiliation: Department of Neurology, University of Heidelberg, Germany.
authors.forename: Lars
authors.initials: L
authors.lastname: Marquardt
authors.forename: Andreas
authors.initials: A
authors.lastname: Ruf
authors.forename: Ulrich
authors.initials: U
authors.lastname: Mansmann
authors.forename: Ralph
authors.initials: R
authors.lastname: Winter
authors.forename: Matthias
authors.initials: M
authors.lastname: Schuler
authors.forename: Florian
authors.initials: F
authors.lastname: Buggle
authors.forename: Horst
authors.initials: H
authors.lastname: Mayer
authors.forename: Armin J
authors.initials: AJ
authors.lastname: Grau
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000378:metabolism*; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D019007:P-Selectin / Q000378:metabolism; D015539:Platelet Activation / Q000502:physiology; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D012016:Reference Values; D012307:Risk Factors; D020521:Stroke / Q000150:complications / Q000378:metabolism*; D060149:Tetraspanin 30
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; C554586:CD63 protein, human; D015815:Cell Adhesion Molecules; D019007:P-Selectin; D010980:Platelet Membrane Glycoproteins; D060149:Tetraspanin 30; D005340:Fibrinogen; D002097:C-Reactive Protein