title: Plasma factor VII-activating protease antigen levels and activity are increased in ischemic stroke.
abstract: BACKGROUND
  Factor VII-activating protease (FSAP) is a recently discovered plasma protease with a role in the regulation of hemostasis and vascular remodeling processes. Higher levels and activity of FSAP have been reported in patients with deep vein thrombosis, but there are no data on plasma FSAP in ischemic stroke (IS).
  
  
  OBJECTIVE
  To investigate whether FSAP antigen levels and activity are associated with IS and/or etiologic subtypes of IS.
  
  
  METHODS
  To assess the potential association between FSAP and IS, plasma FSAP antigen levels and activity were measured in 600 consecutive IS patients and 600 population-based controls from the case-control study the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS). Blood sampling was performed in the acute phase and 3 months after the index stroke. FSAP was also investigated at the genetic level by genotyping of 33 single-nucleotide polymorphisms.
  
  
  RESULTS
  Increased FSAP antigen level and activity, at both time-points, were independently associated with IS. Subtype analysis revealed similar associations for both FSAP measures, at both time-points, in all main IS subtypes. FSAP genotypes showed association with both FSAP plasma measurements, but not with IS.
  
  
  CONCLUSIONS
  Increased plasma FSAP antigen levels and activity were associated with IS and all main etiologic subtypes, suggesting a possible role for FSAP in the pathophysiology of IS, irrespective of the underlying etiology.
authors.affiliation: Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
authors.forename: E
authors.initials: E
authors.lastname: Hanson
authors.forename: S M
authors.initials: SM
authors.lastname: Kanse
authors.forename: A
authors.initials: A
authors.lastname: Joshi
authors.forename: K
authors.initials: K
authors.lastname: Jood
authors.forename: S
authors.initials: S
authors.lastname: Nilsson
authors.forename: C
authors.initials: C
authors.lastname: Blomstrand
authors.forename: C
authors.initials: C
authors.lastname: Jern
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000097:blood / Q000201:enzymology* / Q000453:epidemiology / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D010641:Phenotype; D020641:Polymorphism, Single Nucleotide; D018570:Risk Assessment; D012307:Risk Factors; D012697:Serine Endopeptidases / Q000097:blood* / Q000235:genetics; D020521:Stroke / Q000097:blood / Q000201:enzymology* / Q000453:epidemiology / Q000235:genetics; D013548:Sweden / Q000453:epidemiology; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; C433550:HABP2 protein, human; D012697:Serine Endopeptidases