title: Expression of stromal-cell-derived factor-1 (SDF-1): a predictor of ischaemic stroke?
abstract: OBJECTIVE
  Platelet stromal-cell-derived factor-1 (SDF-1) plays a pivotal role in angiogenesis and the regeneration of ischaemic tissue through the regulation of haematopoietic progenitor cells and is upregulated at the sites of vascular injury and platelet activation. Thus, SDF-1 has recently been discussed as a predictor in ischaemic diseases such as acute myocardial infarction. However, no clinical data pertinent to the investigation of the platelet SDF-1 expression in patients with stroke are available.
  
  
  METHODS
  We consecutively evaluated 196 patients who were admitted to the stroke unit with symptoms suspected for stroke. Surface expression of the platelet activation markers (P-selectin and GPIb) and the expression of platelet-bound SDF-1 were determined by two-colour whole blood flow cytometry.
  
  
  RESULTS
  Patients with transient ischaemic attack (TIA) as well as with ischaemic stroke showed similar levels of SDF-1 expression on hospital admission compared with patients with non-ischaemic (NI) events and with 30 healthy controls (TIA (mean fluorescence intensity±SD): 31.5±18.2 vs. NI: 26.4±15.7; P=0.361; stroke: 28.7±19.8 vs. NI; P=0.943; control: 26.1±11.3; P>0.05 compared with all). Platelet SDF-1 expression showed a trend with the severity of stroke according to National Institute of Health Stroke Scale score (r=0.125; P=0.085), but significantly correlated with the peak levels of C-reactive protein (r=0.218; P=0.002) and with the levels of platelet activation (P-selectin: r=0.389; P=0.001). Multifactorial analysis of covariance revealed a significant influence on platelet SDF-1 expression by smoking (P=0.019).
  
  
  CONCLUSIONS
  Platelet SDF-1 surface expression did not show any significant difference in patients with TIA and ischaemic stroke compared with patients with NI events. Thus, single biomarker evaluation of platelet SDF-1 surface expression is not helpful to predict ischaemic stroke.
authors.affiliation: Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard-Karls-Universität Tübingen, Tübingen, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Wurster
authors.forename: K
authors.initials: K
authors.lastname: Stellos
authors.forename: T
authors.initials: T
authors.lastname: Geisler
authors.forename: P
authors.initials: P
authors.lastname: Seizer
authors.forename: M E
authors.initials: ME
authors.lastname: Andia
authors.forename: A
authors.initials: A
authors.lastname: Schuster
authors.forename: A E
authors.initials: AE
authors.lastname: May
authors.forename: A
authors.initials: A
authors.lastname: Melms
authors.forename: M
authors.initials: M
authors.lastname: Gawaz
authors.forename: B
authors.initials: B
authors.lastname: Bigalke
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood*; D001792:Blood Platelets / Q000378:metabolism; D054377:Chemokine CXCL12 / Q000032:analysis / Q000097:blood*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood / Q000175:diagnosis; D008297:Male; D020521:Stroke / Q000097:blood* / Q000175:diagnosis*
chemical_list: D015415:Biomarkers; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12