Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-1-23
pubmed:abstractText
In the current study, we determined the functional significance of sodium-dependent/-independent glucose transporters at the neurovasculature during oxygen glucose deprivation (OGD). Confluent brain endothelial cells cocultured with astrocytes were exposed to varying degrees of in vitro stroke conditions. Glucose transporter (GLUT) 1 and sodium glucose cotransporter (SGLT) activity were investigated by luminal membrane uptake and transport studies using [(3)H]D-glucose and also by [(14)C]alpha-methyl D-glucopyranoside (AMG), a specific, nonmetabolized substrate of SGLT. In vivo middle cerebral artery occlusion experiments were tested to determine whether blood-brain barrier (BBB) SGLT activity was induced during ischemia. Increases in luminal D-glucose and AMG uptake and transport were observed with in vitro stroke conditions. Specific inhibitor experiments suggest a combined role for both SGLT and GLUT1 at the BBB during OGD. A time-dependent increase in the uptake of AMG was also seen in mice exposed to permanent focal ischemia, and this increase was sensitive to the SGLT inhibitor, phlorizin. Infarct and edema ratio during ischemia were significantly decreased by the inhibition of this transporter. These results show that both GLUT1 and SGLT play a role at the BBB in the blood-to-brain transport of glucose during ischemic conditions, and inhibition of SGLT during stroke has the potential to improve stroke outcome. Pharmacological modulation of this novel BBB transporter could prove to be a brain vascular target in stroke.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-10215638, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-11133510, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-1182174, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-12421352, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-12434396, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-12843224, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-14733905, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-14986005, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-15051802, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-15356425, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-1560234, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-15936510, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-16007500, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-16204409, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-16306934, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-16573648, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-1691534, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-17055160, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-17265689, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-1762065, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-2769254, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-7264642, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-7559210, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-7589845, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-7792078, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8002545, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8371162, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8466186, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8632184, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8786534, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-8955098, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9176146, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9202297, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9518616, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9538503, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9550521, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9596253, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9779189, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9828241, http://linkedlifedata.com/resource/pubmed/commentcorrection/18981287-9886075
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1521-0103
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
328
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
487-95
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
A functional role for sodium-dependent glucose transport across the blood-brain barrier during oxygen glucose deprivation.
pubmed:affiliation
Department of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, Texas 79016, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural