title: Granulocyte-macrophage colony-stimulating factor enhances leptomeningeal collateral growth induced by common carotid artery occlusion.
abstract: OBJECTIVE
  Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been reported to accelerate collateral growth (arteriogenesis) at the circle of Willis in rat brain. However, the effect of GM-CSF on leptomeningeal collateral growth has not been established. We examined the effect of unilateral common carotid artery (CCA) occlusion and GM-CSF treatment on leptomeningeal collateral growth in mice.
  
  
  METHODS
  Adult mice were subjected to unilateral CCA occlusion or sham surgery followed by an alternate-day regimen of GM-CSF (20 microg/kg) or saline injection. On day 7, latex perfusion was performed in 1 set of mice to visualize the leptomeningeal vessels, and the number of Mac-2(+) monocytes/macrophages on the dorsal surface of the brain was counted. In another set of mice, on day 7, permanent ipsilateral middle cerebral artery (MCA) occlusion was performed, and infarct volume was measured.
  
  
  RESULTS
  Leptomeningeal collateral growth was observed after CCA occlusion, and that was enhanced by GM-CSF treatment. An increase in the number of Mac-2(+) cells on the surface of the brain occurred after CCA occlusion and was enhanced by GM-CSF treatment. Seven days after CCA occlusion, GM-CSF treatment decreased the infarct size attributable to subsequent MCA occlusion.
  
  
  CONCLUSIONS
  After CCA occlusion, GM-CSF treatment enhanced leptomeningeal collateral growth and decreased the infarct size after MCA occlusion in mice.
authors.affiliation: Division of Stroke, Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. ktodo@medone.med.osaka-u.ac.jp
authors.forename: Kenichi
authors.initials: K
authors.lastname: Todo
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kitagawa
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Sasaki
authors.forename: Emi
authors.initials: E
authors.lastname: Omura-Matsuoka
authors.forename: Yasukazu
authors.initials: Y
authors.lastname: Terasaki
authors.forename: Naoki
authors.initials: N
authors.lastname: Oyama
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Yagita
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Hori
mesh_terms: D000818:Animals; D001099:Arachnoid / Q000098:blood supply; D001921:Brain / Q000098:blood supply / Q000502:physiology; D020520:Brain Infarction / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D016893:Carotid Stenosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002536:Cerebral Arteries / Q000187:drug effects / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology* / Q000627:therapeutic use; D020925:Hypoxia-Ischemia, Brain / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008578:Meninges / Q000098:blood supply*; D051379:Mice; D008810:Mice, Inbred C57BL; D008833:Microcirculation / Q000187:drug effects* / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000502:physiology; D010841:Pia Mater / Q000098:blood supply; D016896:Treatment Outcome
chemical_list: D016178:Granulocyte-Macrophage Colony-Stimulating Factor