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Conference Paper: Endothelin-1 mediated signaling for increased blood-brain barrier breakdown and infarct after transient focal cerebral ischemia

TitleEndothelin-1 mediated signaling for increased blood-brain barrier breakdown and infarct after transient focal cerebral ischemia
Authors
Keywordsastrocytes
blood–brain barrier
cell death and survival
hypoxia
in-jury
ischemia
trauma
Issue Date2004
PublisherWiley-Blackwell Publishing Ltd.
Citation
The 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 16 Abstract no. C3-4 How to Cite?
AbstractInduced endothelin-1(ET-1) expression was observed in astrocytes after experi-mental ischemic stroke, suggesting a potential role of astrocytic ET-1 in ischemicbrain injury. Previously, we showed that transgenic mice over-expressing ET-1 inastrocytes (GET mice) displayed increased cerebral infarct size and more severeneurological deficits upon focal cerebral ischemia induced by middle cerebralartery occlusion (MCAO). However, the mechanism behind astrocytic ET-1 onischemia-induced brain injury was not clear. Here, expression profile of ET systemwas examined by real-time PCR analyses. In GET brain after MCAO ET-1 levelwas further increased while ET-3 level was lowered. ETA receptor level was up-regulated while ETB receptor level remained unchanged. After MCAO GET brainshowed lower occludin level and increased Evans blue extravasation, indicatingincreased blood–brain barrier (BBB) breakdown which correlated with our resultsthat GET mice displayed increased brain swelling and brain water content. Linearregression analysis also showed correlation of severity of infarction and brainswelling with neurological deficit exacerbation. There was significant p35 down-regulation after MCAO, suggesting involvement of p25/cdk5 cell death pathwayin increased infarct formation. Caspase9 expression was also increased. Theseresults suggested that increased astrocytic ET-1 resulted in BBB disruptionpossibly leading to increased formation of brain edema and swelling, infarct andneurological deficits mediated through cdk5 pathway and, therefore, imposedadverse effects on brain injury after focal cerebral ischemia. Further globalscreening of ET-1-mediated signaling after MCAO will be discussed.Acknowledgements: Supported by RGC and UGC of Hong Kong (AoE/B-15/01).
Persistent Identifierhttp://hdl.handle.net/10722/108829
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorLaw, LPen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-26T00:56:15Z-
dc.date.available2010-09-26T00:56:15Z-
dc.date.issued2004en_HK
dc.identifier.citationThe 6th Biennial Meeting of the Asian-Pacific Society for Neurochemistry, Hong Kong, 4-7 February 2004. In Journal of Neurochemistry, 2004, v. 88 n. S1, p. 16 Abstract no. C3-4-
dc.identifier.issn0022-3042-
dc.identifier.urihttp://hdl.handle.net/10722/108829-
dc.description.abstractInduced endothelin-1(ET-1) expression was observed in astrocytes after experi-mental ischemic stroke, suggesting a potential role of astrocytic ET-1 in ischemicbrain injury. Previously, we showed that transgenic mice over-expressing ET-1 inastrocytes (GET mice) displayed increased cerebral infarct size and more severeneurological deficits upon focal cerebral ischemia induced by middle cerebralartery occlusion (MCAO). However, the mechanism behind astrocytic ET-1 onischemia-induced brain injury was not clear. Here, expression profile of ET systemwas examined by real-time PCR analyses. In GET brain after MCAO ET-1 levelwas further increased while ET-3 level was lowered. ETA receptor level was up-regulated while ETB receptor level remained unchanged. After MCAO GET brainshowed lower occludin level and increased Evans blue extravasation, indicatingincreased blood–brain barrier (BBB) breakdown which correlated with our resultsthat GET mice displayed increased brain swelling and brain water content. Linearregression analysis also showed correlation of severity of infarction and brainswelling with neurological deficit exacerbation. There was significant p35 down-regulation after MCAO, suggesting involvement of p25/cdk5 cell death pathwayin increased infarct formation. Caspase9 expression was also increased. Theseresults suggested that increased astrocytic ET-1 resulted in BBB disruptionpossibly leading to increased formation of brain edema and swelling, infarct andneurological deficits mediated through cdk5 pathway and, therefore, imposedadverse effects on brain injury after focal cerebral ischemia. Further globalscreening of ET-1-mediated signaling after MCAO will be discussed.Acknowledgements: Supported by RGC and UGC of Hong Kong (AoE/B-15/01).-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.-
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.subjectastrocytes-
dc.subjectblood–brain barrier-
dc.subjectcell death and survival-
dc.subjecthypoxia-
dc.subjectin-jury-
dc.subjectischemia-
dc.subjecttrauma-
dc.titleEndothelin-1 mediated signaling for increased blood-brain barrier breakdown and infarct after transient focal cerebral ischemiaen_HK
dc.typeConference_Paperen_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_fulltext-
dc.identifier.doi10.1046/j..2003.0c3_1.x-
dc.identifier.hkuros91236en_HK
dc.identifier.hkuros113553-

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