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Article: Endothelial cell-specific over-expression of endothelin-1 leads to more severe cerebral damage following transient middle cerebral artery occlusion

TitleEndothelial cell-specific over-expression of endothelin-1 leads to more severe cerebral damage following transient middle cerebral artery occlusion
Authors
KeywordsInfarct
Neurological deficit
Stroke
Transgenic mice
Issue Date2004
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 2004, v. 44 SUPPL. 1, p. S293-S300 How to Cite?
AbstractPreviously, we have demonstrated that mRNA expression of endothelin-1 (ET-1), a potent vasoconstrictor, is induced in astrocytes and endothelial cells after ischemic conditions, suggesting that both of these cells synthesize ET-1 under this stress condition. Furthermore, ET-1 protected primary cultured astrocytes from ischemic stress. In order to further investigate the role of endothelial ET-1 in cerebral ischemic injury, transgenic mouse lines (TET) with a transgene that included ET cDNA with SV40 polyA under tyrosine kinase with immunoglobulin and epidermal growth factor homology domain (Tie-1) promoter were used. TET mouse lines were further characterized for ET-1 over-expression in the brain. The reverse transcription-polymerase chain reaction (RT-PCR) analysis using the primers specific for transgene ET-1 showed that transgene ET-1 is only expressed in the brain from TET mice. Total expression of ET-1 mRNA was also increased in the transgenic brain compared with the non-transgenic brain by semi-quantitative RT-PCR. In situ hybridization and immunocytochemical analyses showed that the increased ET-1 mRNA and peptide expressions were detected in endothelial cells of cerebral vessels of TET mice. Under normal conditions, the TET mice that have a slightly increased blood pressure compared with that of non-transgenic mice showed no gross morphological abnormalities in the brain. However, after transient middle cerebral artery occlusion, TET mice showed a more severe neurological deficit, and larger infarct size and volume, suggesting that over-expressing ET-1 in endothelial cells is deleterious to neuronal survival under ischemic conditions. Our present TET model will serve as an ideal model for studying the role of endothelial ET-1 in the pathogenesis of ischemic stroke.
Persistent Identifierhttp://hdl.handle.net/10722/146628
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, JWCen_HK
dc.contributor.authorHo, MCYen_HK
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2012-05-08T03:21:22Z-
dc.date.available2012-05-08T03:21:22Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2004, v. 44 SUPPL. 1, p. S293-S300en_HK
dc.identifier.issn0160-2446en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146628-
dc.description.abstractPreviously, we have demonstrated that mRNA expression of endothelin-1 (ET-1), a potent vasoconstrictor, is induced in astrocytes and endothelial cells after ischemic conditions, suggesting that both of these cells synthesize ET-1 under this stress condition. Furthermore, ET-1 protected primary cultured astrocytes from ischemic stress. In order to further investigate the role of endothelial ET-1 in cerebral ischemic injury, transgenic mouse lines (TET) with a transgene that included ET cDNA with SV40 polyA under tyrosine kinase with immunoglobulin and epidermal growth factor homology domain (Tie-1) promoter were used. TET mouse lines were further characterized for ET-1 over-expression in the brain. The reverse transcription-polymerase chain reaction (RT-PCR) analysis using the primers specific for transgene ET-1 showed that transgene ET-1 is only expressed in the brain from TET mice. Total expression of ET-1 mRNA was also increased in the transgenic brain compared with the non-transgenic brain by semi-quantitative RT-PCR. In situ hybridization and immunocytochemical analyses showed that the increased ET-1 mRNA and peptide expressions were detected in endothelial cells of cerebral vessels of TET mice. Under normal conditions, the TET mice that have a slightly increased blood pressure compared with that of non-transgenic mice showed no gross morphological abnormalities in the brain. However, after transient middle cerebral artery occlusion, TET mice showed a more severe neurological deficit, and larger infarct size and volume, suggesting that over-expressing ET-1 in endothelial cells is deleterious to neuronal survival under ischemic conditions. Our present TET model will serve as an ideal model for studying the role of endothelial ET-1 in the pathogenesis of ischemic stroke.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_HK
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_HK
dc.subjectInfarcten_HK
dc.subjectNeurological deficiten_HK
dc.subjectStrokeen_HK
dc.subjectTransgenic miceen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshBrain - Blood Supply - Pathologyen_US
dc.subject.meshCell Deathen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshEndothelin-1 - Genetics - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Metabolism - Pathologyen_US
dc.subject.meshHippocampus - Blood Supply - Pathologyen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshInfarction, Middle Cerebral Artery - Genetics - Metabolism - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshNerve Degeneration - Genetics - Metabolism - Pathologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSeverity Of Illness Indexen_US
dc.subject.meshUp-Regulationen_US
dc.titleEndothelial cell-specific over-expression of endothelin-1 leads to more severe cerebral damage following transient middle cerebral artery occlusionen_HK
dc.typeArticleen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/01.fjc.0000166277.70538.b0en_HK
dc.identifier.pmid15838304-
dc.identifier.scopuseid_2-s2.0-11144336680en_HK
dc.identifier.hkuros106082-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-11144336680&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issueSUPPL. 1en_HK
dc.identifier.spageS293en_HK
dc.identifier.epageS300en_HK
dc.identifier.isiWOS:000226099000073-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung, JWC=8978634300en_HK
dc.identifier.scopusauthoridHo, MCY=7403080620en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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