title: Expression of glucose transporter-1 and aquaporin-4 in the cerebral cortex of stroke-prone spontaneously hypertensive rats in relation to the blood-brain barrier function.
abstract: BACKGROUND
  Cerebral edema is an important initial event in cases of stroke among humans. Although hypertension is a major risk factor for endothelial injury, the precise mechanisms regulating brain microvascular changes are still unknown. To elucidate the pathogenesis of increases in vascular permeability in the cerebral cortex, we investigated the expression of glucose transporter-1 (GLUT-1) in endothelial cells and aquaporin-4 (AQP4) in astrocytes in relation to blood-brain barrier (BBB) function.
  
  
  METHODS
  Using male stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY), the particular localization of both GLUT-1 and AQP4 was investigated by immunohistochemistry. Quantitative changes in these molecules were examined by Western blot analysis in these rats at 6 weeks and 20 weeks of age. Furthermore, to investigate the expression of these molecules at the mRNA level, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was carried out using 20-week-old SHRSP and age-matched WKY.
  
  
  RESULTS
  We confirmed the localization of GLUT-1 in endothelial cells and that of AQP4 in the end feet of astrocytes around microvessels, as determined by electron immunohistochemistry. No significant differences were found in the expression of these molecules in rats at 6 weeks of age, whereas GLUT-1 expression was lower, but that of AQP4 was higher, in SHRSP after the establishment of hypertension. Furthermore, GLUT-1 mRNA expression was lower in SHRSP, and AQP4 mRNA expression was also lower in SHRSP than in WKY at 20 weeks of age.
  
  
  CONCLUSIONS
  These results indicate that AQP4 may play a much more important role in BBB function than GLUT-1, and thereby also in water distribution in the cerebral cortex of SHRSP with severe hypertension.
authors.affiliation: Department of Pathology, Kinki University School of Medicine, Osaka-sayama, Osaka 589-8511, Japan. hiroyuki@med.kindai.ac.jp
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ishida
authors.forename: Kumiko
authors.initials: K
authors.lastname: Takemori
authors.forename: Kensaku
authors.initials: K
authors.lastname: Dote
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ito
mesh_terms: D000818:Animals; D051401:Aquaporin 4 / Q000032:analysis* / Q000235:genetics; D001253:Astrocytes / Q000737:chemistry; D001812:Blood-Brain Barrier / Q000502:physiology*; D015153:Blotting, Western; D002199:Capillary Permeability; D002540:Cerebral Cortex / Q000098:blood supply / Q000737:chemistry* / Q000473:pathology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology; D005786:Gene Expression Regulation; D051272:Glucose Transporter Type 1 / Q000032:analysis* / Q000235:genetics; D006973:Hypertension / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D008854:Microscopy, Electron; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020521:Stroke / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: C496032:Aqp4 protein, rat; D051401:Aquaporin 4; D051272:Glucose Transporter Type 1; D012333:RNA, Messenger