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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

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
Authors
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
Citation
Brain Research, 2009, v. 1266, p. 121-129 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/146632
ISSN
2014 Impact Factor: 2.843
2013 SCImago Journal Rankings: 1.572
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, JWCen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-08T03:21:23Z-
dc.date.available2012-05-08T03:21:23Z-
dc.date.issued2009en_HK
dc.identifier.citationBrain Research, 2009, v. 1266, p. 121-129en_HK
dc.identifier.issn0006-8993en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146632-
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.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/brainresen_HK
dc.relation.ispartofBrain Researchen_HK
dc.subjectBlood-brain barrieren_HK
dc.subjectEndothelial receptoren_HK
dc.subjectIschemiaen_HK
dc.subjectStrokeen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshAquaporin 4 - Metabolismen_US
dc.subject.meshBlood-Brain Barrier - Pathology - Physiopathologyen_US
dc.subject.meshBrain - Blood Supply - Pathology - Physiopathologyen_US
dc.subject.meshCapillary Permeabilityen_US
dc.subject.meshEndothelin-1 - Genetics - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Pathology - Physiopathologyen_US
dc.subject.meshImmunoglobulins - Metabolismen_US
dc.subject.meshInfarction, Middle Cerebral Artery - Pathology - Physiopathologyen_US
dc.subject.meshMatrix Metalloproteinase 2 - Metabolismen_US
dc.subject.meshMembrane Glycoproteins - Metabolismen_US
dc.subject.meshMembrane Proteins - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshNadph Oxidase - Metabolismen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshPyrrolidines - Administration & Dosageen_US
dc.subject.meshReceptor, Endothelin A - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshReceptor, Tie-1 - Geneticsen_US
dc.subject.meshSuperoxides - Metabolismen_US
dc.subject.meshTyrosine - Analogs & Derivatives - Metabolismen_US
dc.subject.meshWater - Metabolismen_US
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 occlusionen_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.brainres.2009.01.070en_HK
dc.identifier.pmid19230825en_HK
dc.identifier.scopuseid_2-s2.0-63449101376en_HK
dc.identifier.hkuros167833-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-63449101376&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1266en_HK
dc.identifier.spage121en_HK
dc.identifier.epage129en_HK
dc.identifier.isiWOS:000265768600013-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLeung, JWC=8978634300en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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