title: Dysregulated survivin expression in nasal polyps of individuals with aspirin exacerbated respiratory disease.
abstract: BACKGROUND
  A derailed balance of cell proliferation and apoptosis is presumed to result in cell hyperplasia as a typical feature of nasal polyps. Survivin, a protein of the inhibitors of the apoptosis family is proposed to promote polyp formation. However, studies concerning  survivin expression in chronic rhinosinusitis (CRS) with nasal polyps are rare and the specificity of the survivin expression in nasal polyps from individuals with aspirin-exacerbated respiratory disease (AERD) has not been investigated.
  
  
  METHODS
  Immunohistochemical survivin  expression analysis was performed. Samples were taken from the ethmoid sinus of individuals with CRS with nasal polyps with and without AERD during sinus surgery and control specimens of the inferior turbinate from individuals without CRS. Cell cultures were stimulated with recombinant vascular  endothelial growth factor (VEGF(165)) and the resulting survivin expression was analyzed by Western blot.
  
  
  RESULTS
  The survivin expression of 61 specimens was analyzed by quantitative immunohistochemistry and a potential VEGF-dependant stimulation of survivin in  cell cultures was investigated. The survivin expression in nasal polyps from individuals with AERD was increased compared with the controls (median, 1194 versus 927 arbitrary units [A.U.]; p = 0.054). Western blot analysis revealed in vitro a VEGF-dependant regulation of survivin in  nasal polyps from individuals without AERD, but not in those with AERD (p = 0.05).
  
  
  CONCLUSIONS
  Enhanced survivin expression might result in decreased apoptosis and cellular hyperplasia as a part of the largely unknown pathophysiology of nasal polyp formation. Furthermore,  we hypothesize a pathological, VEGF-independent constitutive survivin expression in nasal polyps of individuals with AERD.
authors.affiliation: Department of Otolaryngology, Head and Neck Surgery, University Medical Center, Johannes Gutenberg University, Mainz, Germany. kai.fruth@unimedizin-mainz.de
authors.forename: Kai
authors.initials: K
authors.lastname: Fruth
authors.forename: Eduard
authors.initials: E
authors.lastname: Schramek
authors.forename: Dominic
authors.initials: D
authors.lastname: Docter
authors.forename: Boris R
authors.initials: BR
authors.lastname: Haxel
authors.forename: Astrid
authors.initials: A
authors.lastname: Schneider
authors.forename: Wolf J
authors.initials: WJ
authors.lastname: Mann
authors.forename: Juergen
authors.initials: J
authors.lastname: Brieger
mesh_terms: D000328:Adult; D017209:Apoptosis; D001241:Aspirin / Q000009:adverse effects*; D002478:Cells, Cultured; D002908:Chronic Disease; D018450:Disease Progression; D004342:Drug Hypersensitivity / Q000378:metabolism*; D005005:Ethmoid Sinus / Q000276:immunology; D005260:Female; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000096:biosynthesis*; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000378:metabolism*; D012220:Rhinitis / Q000378:metabolism*; D012852:Sinusitis / Q000378:metabolism*; D000077022:Survivin; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D055815:Young Adult
chemical_list: C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D000077022:Survivin; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D001241:Aspirin