title: Proliferation of vascular smooth muscle cells in glioblastoma multiforme.
abstract: OBJECTIVE
  Glioblastomas multiforme (GBM) contain a higher number of alpha-smooth muscle actin (SMA)-positive vascular smooth muscle cells (VSMCs) than those in the respective normal neuronal tissue. The role of VSMCs during angiogenesis is unclear, and it is also uncertain whether and to what extent angiogenic factors might be involved in GBM VSMCs. In GBMs, the contribution of VSMCs in angiogenesis accompanying endothelial proliferation and the correlation of VSMC proliferation with vascular endothelial growth factor (VEGF) expression were examined using an immunohistochemical method.
  
  
  METHODS
  The examined material, including surrounding brain tissue, came from 12 cases (6 men and 6 women) with classic GBM. Microvessel densities (MVDs) of CD31-immunoreactive vessels (CD31-MVD) and SMA-immunoreactive vessels (SMA-MVD) were obtained in areas selected from white matter, boundary, tumor (concentrated area of tumor cells), and perinecrosis. Subsequently, the SMA-MVD/CD31-MVD (SMA/CD31) rate, representing the percentage of vessels with VSMCs in the region, was calculated in each area. The VEGF immunoreactivity of tumor cells was examined, and cases were divided into 2 groups: < 30% VEGF expression of tumor cells (low VEGF group) and > 30% VEGF expression of tumor cells (high VEGF group).
  
  
  RESULTS
  The SMA/CD31 rate of the boundary was significantly lower than that of the tumor (p < 0.005) and perinecrosis (p < 0.001). The SMA/CD31 rate of the high VEGF group was significantly higher than that of the low VEGF group (p < 0.05) in the tumor.
  
  
  CONCLUSIONS
  In GBMs, the transformation and proliferation of VSMCs may accompany neovascularization and may also be induced by angiogenic factors.
authors.affiliation: Department of Neurosurgery, Faculty of Medical Sciences, University of Fukui, Japan. takeu@u-fukui.ac.jp
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Takeuchi
authors.forename: Norichika
authors.initials: N
authors.lastname: Hashimoto
authors.forename: Ryuhei
authors.initials: R
authors.lastname: Kitai
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Kubota
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Kikuta
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D001932:Brain Neoplasms / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division / Q000502:physiology; D005260:Female; D005909:Glioblastoma / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D008279:Magnetic Resonance Imaging; D008297:Male; D008833:Microcirculation / Q000502:physiology; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000473:pathology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D055815:Young Adult
chemical_list: D000199:Actins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A