title: Soluble adhesion molecules reflect endothelial cell activation in ischemic stroke and in carotid atherosclerosis.
abstract: OBJECTIVE
  Activation of endothelial cells and platelets plays an important role in the development of atherosclerosis and thrombotic disorders. Soluble adhesion molecules originating from these cells can be demonstrated in plasma. We hypothesized that elevated plasma concentrations of soluble P-selectin (sP-selectin), soluble intercellular adhesion mole-cule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble E-selectin (sE-selectin) can reflect activation of endothelial cells and/or platelets in acute ischemic stroke and in previously symptomatic internal carotid artery stenosis.
  
  
  METHODS
  Plasma was sampled from patients within 2 days of acute ischemic stroke (n = 28), from patients with a previous (> 1 week) transient or persistent ischemic neurological deficit associated with stenosis of the internal carotid artery (n = 34), and from control patients without a history of vascular disease (n = 34). Concentrations of sP-selectin, sICAM-1, sVCAM-1, and sE-selectin were measured by means of an enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Compared with control subjects, sP-selectin and sE-selectin were significantly elevated in the acute stage of ischemic stroke (P < .0001 and P = .001, respectively) as well as in previously symptomatic carotid stenosis (P < .0001 and P = .0007). sICAM-1 and sVCAM-1 were not increased.
  
  
  CONCLUSIONS
  The elevated levels of sE-selectin indicate that endothelial cell activation occurs both in the acute stage of ischemic stroke and in previously symptomatic carotid atherosclerosis. Increased sP-selectin concentrations reflect endothelial cell activation as well but may also be caused by platelet activation.
authors.affiliation: Department of Neurology, University Hospital Utrecht, Netherlands. C.Frijns@neuro.azu.nl
authors.forename: C J
authors.initials: CJ
authors.lastname: Frijns
authors.forename: L J
authors.initials: LJ
authors.lastname: Kappelle
authors.forename: J
authors.initials: J
authors.lastname: van Gijn
authors.forename: H K
authors.initials: HK
authors.lastname: Nieuwenhuis
authors.forename: J J
authors.initials: JJ
authors.lastname: Sixma
authors.forename: R
authors.initials: R
authors.lastname: Fijnheer
mesh_terms: D001161:Arteriosclerosis / Q000473:pathology / Q000503:physiopathology*; D001792:Blood Platelets / Q000502:physiology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002340:Carotid Artery Diseases / Q000473:pathology / Q000503:physiopathology*; D015815:Cell Adhesion Molecules / Q000097:blood*; D002561:Cerebrovascular Disorders / Q000473:pathology / Q000503:physiopathology*; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D009994:Osmolar Concentration; D012995:Solubility; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1