title: Compensatory neovascularization after cauda equina compression in rats.
abstract: METHODS
  An experimental study of compensatory neovascularization after cauda equina compression in rats.
  
  
  OBJECTIVE
  To explore the possibility that cauda equina compression induces compensatory neovascularization accompanied by an increase in the expression of vascular endothelial growth factor (VEGF).
  
  
  BACKGROUND
  VEGF is a potent promoter of neovascularization that follows ischemia. Studies suggest that compression of the cauda equina causes ischemic changes that in turn cause an increase in VEGF expression that induces neovascularization. The mechanisms by which neovascularization develops in a compressed cauda equina are unknown.
  
  
  METHODS
  Two rectangular-solid pieces of silicone rubber were implanted in the fourth and sixth epidural spaces of rats (1 piece in each space); in the sham control group, no rubber was implanted. VEGF expression in the compressed cauda equina was assessed by immunohistochemistry and Western blotting. Ischemia and neovascularization of the cauda equina were assessed by immunostaining for hypoxia-inducible factor-1 alpha (HIF-1 alpha) and 5-bromodeoxyuridine (BrdU). The unpaired Student t test was used for statistical analysis (P < 0.05).
  
  
  RESULTS
  At 14 and 21 days after surgery, ischemic changes were observed, as indicated by expression of HIF-1 alpha. In the compression group at 21 and 28 days after surgery, Western blot analysis showed a significant increase in VEGF expression (P < 0.05). VEGF was localized to pericytes, Schwann cells, and macrophages. In the compression group at 21 days after surgery, neovascularization was observed, as indicated by an increase in the number of proliferating endothelial cells (which stained positive for BrdU).
  
  
  CONCLUSIONS
  Cauda equina compression seems to induce compensatory neovascularization of the cauda equina accompanied by an increase in VEGF expression.
authors.affiliation: Department of Orthopedic surgery, University of the Ryukyus, Okinawa, Japan. yonnyb8@hotmail.com
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yonetake
authors.forename: Miho
authors.initials: M
authors.lastname: Sekiguchi
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Konno
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Kikuchi
authors.forename: Fuminori
authors.initials: F
authors.lastname: Kanaya
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000032:analysis; D015153:Blotting, Western; D001973:Bromodeoxyuridine / Q000032:analysis; D002420:Cauda Equina / Q000737:chemistry / Q000473:pathology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D005260:Female; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000032:analysis; D007124:Immunoenzyme Techniques; D018919:Neovascularization, Physiologic; D051381:Rats; D017207:Rats, Sprague-Dawley; D013130:Spinal Stenosis / Q000473:pathology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D015415:Biomarkers; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D042461:Vascular Endothelial Growth Factor A; D001973:Bromodeoxyuridine