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Article: Endothelial endothelin-1 over-expression using receptor tyrosine kinase tie-1 promoter leads to more severe vascular permeability and blood brain barrier breakdown after transient middle cerebral artery occlusion
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TitleEndothelial endothelin-1 over-expression using receptor tyrosine kinase tie-1 promoter leads to more severe vascular permeability and blood brain barrier breakdown after transient middle cerebral artery occlusion
 
AuthorsLeung, JWC1
Chung, SSM1
Chung, SK1
 
KeywordsBlood-brain barrier
Endothelial receptor
Ischemia
Stroke
 
Issue Date2009
 
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
 
CitationBrain Research, 2009, v. 1266, p. 121-129 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.brainres.2009.01.070
 
AbstractEndothelin-1 (ET-1) is up-regulated in the endothelial cells and astrocytes under ischemia. Transgenic mice with astrocytic ET-1 over-expression (GET-1) showed more severe neurological deficit and larger infarct after transient middle cerebral artery occlusion (MCAO). Here, the significance of endothelial ET-1 in ischemic brain injury was investigated using transgenic mice with the endothelial ET-1 over-expression (TET-1). Increased ET-1 level was observed in the TET-1 brain infarct core after transient MCAO. ET A receptor expression was induced in the penumbra and ET A antagonist (A-147627) partially normalized the infarct volume and neurological deficit. In the infarct core of TET-1 brain, superoxide, nitrotyrosine, and gp91 phox levels were increased. TET-1 brain displayed increased matrix metalloproteinase-2 expression, water content, immunoglobulin leakage and decreased occludin level in the ipsilateral hemisphere indicative of BBB breakdown and hemispheric edema. Interestingly, AQP-4 expression was increased in the penumbra of TET-1 brain following transient MCAO leading to the water accumulation. Taken together, endothelial ET-1 over-expression and ETA receptor activation contributes to the increased oxidative stress, water accumulation and BBB breakdown after transient MCAO leading to more severe neurological deficit and increased infarct. © 2008 Elsevier B.V. All rights reserved.
 
ISSN0006-8993
2012 Impact Factor: 2.879
2012 SCImago Journal Rankings: 1.217
 
DOIhttp://dx.doi.org/10.1016/j.brainres.2009.01.070
 
ISI Accession Number IDWOS:000265768600013
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLeung, JWC
 
dc.contributor.authorChung, SSM
 
dc.contributor.authorChung, SK
 
dc.date.accessioned2012-05-08T03:21:23Z
 
dc.date.available2012-05-08T03:21:23Z
 
dc.date.issued2009
 
dc.description.abstractEndothelin-1 (ET-1) is up-regulated in the endothelial cells and astrocytes under ischemia. Transgenic mice with astrocytic ET-1 over-expression (GET-1) showed more severe neurological deficit and larger infarct after transient middle cerebral artery occlusion (MCAO). Here, the significance of endothelial ET-1 in ischemic brain injury was investigated using transgenic mice with the endothelial ET-1 over-expression (TET-1). Increased ET-1 level was observed in the TET-1 brain infarct core after transient MCAO. ET A receptor expression was induced in the penumbra and ET A antagonist (A-147627) partially normalized the infarct volume and neurological deficit. In the infarct core of TET-1 brain, superoxide, nitrotyrosine, and gp91 phox levels were increased. TET-1 brain displayed increased matrix metalloproteinase-2 expression, water content, immunoglobulin leakage and decreased occludin level in the ipsilateral hemisphere indicative of BBB breakdown and hemispheric edema. Interestingly, AQP-4 expression was increased in the penumbra of TET-1 brain following transient MCAO leading to the water accumulation. Taken together, endothelial ET-1 over-expression and ETA receptor activation contributes to the increased oxidative stress, water accumulation and BBB breakdown after transient MCAO leading to more severe neurological deficit and increased infarct. © 2008 Elsevier B.V. All rights reserved.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationBrain Research, 2009, v. 1266, p. 121-129 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.brainres.2009.01.070
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.brainres.2009.01.070
 
dc.identifier.epage129
 
dc.identifier.hkuros167833
 
dc.identifier.isiWOS:000265768600013
 
dc.identifier.issn0006-8993
2012 Impact Factor: 2.879
2012 SCImago Journal Rankings: 1.217
 
dc.identifier.pmid19230825
 
dc.identifier.scopuseid_2-s2.0-63449101376
 
dc.identifier.spage121
 
dc.identifier.urihttp://hdl.handle.net/10722/146632
 
dc.identifier.volume1266
 
dc.languageeng
 
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainres
 
dc.publisher.placeNetherlands
 
dc.relation.ispartofBrain Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshAquaporin 4 - Metabolism
 
dc.subject.meshBlood-Brain Barrier - Pathology - Physiopathology
 
dc.subject.meshBrain - Blood Supply - Pathology - Physiopathology
 
dc.subject.meshCapillary Permeability
 
dc.subject.meshEndothelin-1 - Genetics - Metabolism
 
dc.subject.meshEndothelium, Vascular - Pathology - Physiopathology
 
dc.subject.meshImmunoglobulins - Metabolism
 
dc.subject.meshInfarction, Middle Cerebral Artery - Pathology - Physiopathology
 
dc.subject.meshMatrix Metalloproteinase 2 - Metabolism
 
dc.subject.meshMembrane Glycoproteins - Metabolism
 
dc.subject.meshMembrane Proteins - Metabolism
 
dc.subject.meshMice
 
dc.subject.meshMice, Transgenic
 
dc.subject.meshNadph Oxidase - Metabolism
 
dc.subject.meshOxidative Stress
 
dc.subject.meshPromoter Regions, Genetic
 
dc.subject.meshPyrrolidines - Administration & Dosage
 
dc.subject.meshReceptor, Endothelin A - Antagonists & Inhibitors - Metabolism
 
dc.subject.meshReceptor, Tie-1 - Genetics
 
dc.subject.meshSuperoxides - Metabolism
 
dc.subject.meshTyrosine - Analogs & Derivatives - Metabolism
 
dc.subject.meshWater - Metabolism
 
dc.subjectBlood-brain barrier
 
dc.subjectEndothelial receptor
 
dc.subjectIschemia
 
dc.subjectStroke
 
dc.titleEndothelial endothelin-1 over-expression using receptor tyrosine kinase tie-1 promoter leads to more severe vascular permeability and blood brain barrier breakdown after transient middle cerebral artery occlusion
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong