title: Expression of vascular endothelial growth factor receptors in experimental otitis media in the rat.
abstract: OBJECTIVE
  Increased vascular permeability and endothelial cell growth are important in the pathogenesis of otitis media with effusion (OME) and vascular endothelial growth factor (VEGF) is known to play an important role in the increased vascular permeability and angiogenesis associated with OME. The action of VEGF is mediated by two different high-affinity receptors--VEGF receptor-1 (VEGFR-1; flm-like tyrosine kinase-1; flt-1) and VEGFR-2 (kinase insert domain-containing receptor; flk-1)--predominantly located on the vascular endothelium. The purpose of this study was to investigate the expression of three forms of VEGFR (-1, -2 and -3) in an endotoxin-induced rat model of OME.
  
  
  METHODS
  Middle ear mucosa were obtained at 0, 1, 3, 6 and 12 h and 1, 3, 7 and 14 days after induction, and the expression of VEGFR mRNA and protein was evaluated using semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting.
  
  
  RESULTS
  RT-PCR revealed that the expression of VEGFR-1 and -2 mRNA was upregulated between 1 h and 3 days after endotoxin instillation, with peak expression occurring at 12 h and on Day 1. No expression of VEGFR-3 mRNA was detected in any of the samples. Expression patterns of VEGFR-1 and -2 protein observed by Western blotting were similar to those of VEGFR-1 and -2 mRNA and peak expression was observed on Day 1. Expression of VEGFR mRNA or protein was not detected in either normal or saline-instilled middle ear mucosa.
  
  
  CONCLUSIONS
  These results suggest that both VEGFR-1 and -2 are upregulated during experimental otitis media in the rat and these receptors may play different roles in the production of effusion in OME.
authors.affiliation: Department of Otolaryngology--Head and Neck Surgery, Korea University College of Medicine, Seoul, South Korea.
authors.forename: Sung Won
authors.initials: SW
authors.lastname: Chae
authors.forename: Seo Jin
authors.initials: SJ
authors.lastname: Kim
authors.forename: Jeung Lim
authors.initials: JL
authors.lastname: Kim
authors.forename: Hak Hyun
authors.initials: HH
authors.lastname: Jung
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology; D004731:Endotoxins; D005786:Gene Expression Regulation; D009092:Mucous Membrane / Q000098:blood supply / Q000737:chemistry; D010034:Otitis Media with Effusion / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D040262:Receptors, Vascular Endothelial Growth Factor / Q000032:analysis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000032:analysis; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000032:analysis; D040321:Vascular Endothelial Growth Factor Receptor-3 / Q000032:analysis
chemical_list: D004731:Endotoxins; D012333:RNA, Messenger; D040262:Receptors, Vascular Endothelial Growth Factor; D040281:Vascular Endothelial Growth Factor Receptor-1; D040301:Vascular Endothelial Growth Factor Receptor-2; D040321:Vascular Endothelial Growth Factor Receptor-3