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Conference Paper: Endothelin-1 leads to increased necrotic cell density in the brain after transient focal cerebral ischemia

TitleEndothelin-1 leads to increased necrotic cell density in the brain after transient focal cerebral ischemia
Authors
KeywordsSTROKE
CEREBRAL BLOOD FLOW
MCAO
MOUSE
Issue Date2001
Citation
Neuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 206.12 How to Cite?
AbstractA transgenic (Tg) mouse model was developed to study the role of astrocytic endothelin-1 (ET-1) in cerebral injury. We have previously shown that this over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain since no gross abnormalities were observed in Tg mouse brains. However, Tg mice displayed an increase in cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) as reported previously. By quantitative PCR analyses, we observed that wildtype (WT) animals displayed a 2.5 fold increase in ET-1 mRNA levels in the ipsilateral brain after MCAO as we expected whereas Tg mice showed a 17.5 fold increase in ET-1 mRNA levels when compared to WT animals under both sham-operation and MCAO. Interestingly, when we examined the brain sections of the MCAO animals, we observed that there were fewer apoptotic cells but more necrotic cells in the lesion core of cerebral infarct regions in Tg mice when compared to their WT littermates. Our data suggested that ET-1 overexpression resulted in larger infarct size with more severe neurological deficits and increased cell death after MCAO. Yet, the relatively higher density of necrotic vs. apoptotic cells in the lesion core suggested that ET-1 may contribute to increased necrotic cell density in the brain after transient focal cerebral ischemia. Supported by Research Grants Council (Hong Kong)
Persistent Identifierhttp://hdl.handle.net/10722/108835

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorChen, AYSen_HK
dc.contributor.authorHo, MCYen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-26T00:56:30Z-
dc.date.available2010-09-26T00:56:30Z-
dc.date.issued2001en_HK
dc.identifier.citationNeuroscience 2001, San Diego, CA, 10-15 November 2001, Presentation no. 206.12-
dc.identifier.urihttp://hdl.handle.net/10722/108835-
dc.description.abstractA transgenic (Tg) mouse model was developed to study the role of astrocytic endothelin-1 (ET-1) in cerebral injury. We have previously shown that this over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain since no gross abnormalities were observed in Tg mouse brains. However, Tg mice displayed an increase in cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO) as reported previously. By quantitative PCR analyses, we observed that wildtype (WT) animals displayed a 2.5 fold increase in ET-1 mRNA levels in the ipsilateral brain after MCAO as we expected whereas Tg mice showed a 17.5 fold increase in ET-1 mRNA levels when compared to WT animals under both sham-operation and MCAO. Interestingly, when we examined the brain sections of the MCAO animals, we observed that there were fewer apoptotic cells but more necrotic cells in the lesion core of cerebral infarct regions in Tg mice when compared to their WT littermates. Our data suggested that ET-1 overexpression resulted in larger infarct size with more severe neurological deficits and increased cell death after MCAO. Yet, the relatively higher density of necrotic vs. apoptotic cells in the lesion core suggested that ET-1 may contribute to increased necrotic cell density in the brain after transient focal cerebral ischemia. Supported by Research Grants Council (Hong Kong)-
dc.languageengen_HK
dc.relation.ispartofSociety for Neuroscience Annual Meetingen_HK
dc.subjectSTROKE-
dc.subjectCEREBRAL BLOOD FLOW-
dc.subjectMCAO-
dc.subjectMOUSE-
dc.titleEndothelin-1 leads to increased necrotic cell density in the brain after transient focal cerebral ischemiaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailChen, AYS: ayschen@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.hkuros68596en_HK
dc.publisher.placeSociety for Neuroscience-

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