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Conference Paper: Endothelin-1 over-expression leads to blood-brain barrier disruption resulting in increased infarct and edema after focal ischemia

TitleEndothelin-1 over-expression leads to blood-brain barrier disruption resulting in increased infarct and edema after focal ischemia
Authors
KeywordsBrain damage
GFAP
Hypoxia/ischemia
Neurotrauma
Stroke
Issue Date2003
PublisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159
Citation
Journal of Neurochemistry, 2003, v. 87 suppl. 1, p. 142, abstract no. P13-66 How to Cite?
AbstractInduced endothelin-1 (ET-1) expression was observed in astrocytes after experimental ischemic stroke, suggesting a potential role of astrocytic ET-1 in ischemic brain injury. Previously, we showed that transgenic mice over-expressing ET-1 in astrocytes (GET mice) displayed increased cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Here, the expression profile of the endothelin system was examined in GET mouse brains after MCAO. Quantitative real-time PCR analyses showed that ET-1 mRNA levels in GET ipsilateral mouse brain after MCAO was further increased, while ET-3 levels stayed relatively constant when compared with sham-operated animals. There was an up-regulation of ETA receptor mRNA levels in GET ipsilateral brains while ETB receptor mRNA levels remained unchanged. In addition, Evans blue extravasation studies showed increased blood–brain barrier (BBB) breakdown in GET mice after MCAO, correlating with our findings that GET mice displayed increased brain swelling and brain water content. Moreover, linear regression analysis showed that severity of infarction and brain swelling correlated with the exacerbation of neurologic deficits. These results suggested that increased astrocytic ET-1 resulted in more BBB disruption leading to increased formation of brain edema, infarct and neurologic deficits after focal cerebral ischemia.
DescriptionPoster Session P13: Neurotoxicity, Neurodegeneration, Neuroprotection, Ischemia/Hypoxia and Apoptosis
Persistent Identifierhttp://hdl.handle.net/10722/88053
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorLo, ACY-
dc.contributor.authorChung, SSM-
dc.contributor.authorChung, SK-
dc.date.accessioned2010-09-06T09:38:02Z-
dc.date.available2010-09-06T09:38:02Z-
dc.date.issued2003-
dc.identifier.citationJournal of Neurochemistry, 2003, v. 87 suppl. 1, p. 142, abstract no. P13-66-
dc.identifier.issn0022-3042-
dc.identifier.urihttp://hdl.handle.net/10722/88053-
dc.descriptionPoster Session P13: Neurotoxicity, Neurodegeneration, Neuroprotection, Ischemia/Hypoxia and Apoptosis-
dc.description.abstractInduced endothelin-1 (ET-1) expression was observed in astrocytes after experimental ischemic stroke, suggesting a potential role of astrocytic ET-1 in ischemic brain injury. Previously, we showed that transgenic mice over-expressing ET-1 in astrocytes (GET mice) displayed increased cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Here, the expression profile of the endothelin system was examined in GET mouse brains after MCAO. Quantitative real-time PCR analyses showed that ET-1 mRNA levels in GET ipsilateral mouse brain after MCAO was further increased, while ET-3 levels stayed relatively constant when compared with sham-operated animals. There was an up-regulation of ETA receptor mRNA levels in GET ipsilateral brains while ETB receptor mRNA levels remained unchanged. In addition, Evans blue extravasation studies showed increased blood–brain barrier (BBB) breakdown in GET mice after MCAO, correlating with our findings that GET mice displayed increased brain swelling and brain water content. Moreover, linear regression analysis showed that severity of infarction and brain swelling correlated with the exacerbation of neurologic deficits. These results suggested that increased astrocytic ET-1 resulted in more BBB disruption leading to increased formation of brain edema, infarct and neurologic deficits after focal cerebral ischemia.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159-
dc.relation.ispartofJournal of Neurochemistry-
dc.subjectBrain damage-
dc.subjectGFAP-
dc.subjectHypoxia/ischemia-
dc.subjectNeurotrauma-
dc.subjectStroke-
dc.titleEndothelin-1 over-expression leads to blood-brain barrier disruption resulting in increased infarct and edema after focal ischemia-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3042&volume=87&spage=142 Suppl. 1&epage=&date=2003&atitle=Endothelin-1+over-expression+leads+to+blood-brain+barrier+disruption+resulting+in+increased+infarct+and+edema+after+focal+ischemiaen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hk-
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityLo, ACY=rp00425-
dc.identifier.authorityChung, SSM=rp00376-
dc.identifier.authorityChung, SK=rp00381-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1046/j.1474-1644.2003.2175_13.x-
dc.identifier.hkuros113550-
dc.identifier.volume87-
dc.identifier.issuesuppl. 1-
dc.identifier.spage142, abstract no. P13-66-
dc.identifier.epage142, abstract no. P13-66-
dc.publisher.placeUnited Kingdom-

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