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Conference Paper: Endothelin-1 overexpression leads to blood-brain barrier disruption, more brain edema and increased aquaporin 4 expression in astrocytic processes after experimental stroke

TitleEndothelin-1 overexpression leads to blood-brain barrier disruption, more brain edema and increased aquaporin 4 expression in astrocytic processes after experimental stroke
Authors
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
The Hong Kong Society of Neurosciences 24th Annual Scientific Meeting, Hong Kong, 13-14 January 2005. In Neurosignals, 2006, v. 15 n. 3, p. 127 How to Cite?
AbstractUnder normal condition endothelin-1 (ET-1) is expressed by cerebral endothelial cells. However, increased level of ET-1 was observed in both astrocytes and endothelial cells after experimental ischemic stroke and hypoxia/ischemia, suggesting a potential role of astrocytic and endothelial ET-1 in ischemic brain injury. Previously, we reported that transgenic mice over-expressing ET-1 in astrocytes (GET-1 mice) displayed increased cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). However, the mechanism behind astrocytic ET-1 on ischemia-induced brain injury was not clear. Here, we report that GET mice showed lower occludin levels and increased Evans blue extravasation, suggesting increased blood-brain barrier (BBB) breakdown in GET-1 mice after MCAO. GET-1 mice also displayed increased brain swelling and brain water content together with decreased occludin and up-regulated aquaporin 4 expression. These results suggested that increased astrocytic ET-1 resulted in BBB disruption leading to increased formation of brain edema and swelling, infarct and neurological deficits and therefore imposed adverse effects on brain injury after focal cerebral ischemia. Acknowledgement: Supported by Research Grants Council and Area of Excellence from University Grants Council of Hong Kong (AoE/B-15/01).
Persistent Identifierhttp://hdl.handle.net/10722/108807
ISSN
2014 Impact Factor: 2.000
2014 SCImago Journal Rankings: 0.952

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorFung, KLen_HK
dc.contributor.authorYaw, LPen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-26T00:55:17Z-
dc.date.available2010-09-26T00:55:17Z-
dc.date.issued2006en_HK
dc.identifier.citationThe Hong Kong Society of Neurosciences 24th Annual Scientific Meeting, Hong Kong, 13-14 January 2005. In Neurosignals, 2006, v. 15 n. 3, p. 127-
dc.identifier.issn1424-862X-
dc.identifier.urihttp://hdl.handle.net/10722/108807-
dc.description.abstractUnder normal condition endothelin-1 (ET-1) is expressed by cerebral endothelial cells. However, increased level of ET-1 was observed in both astrocytes and endothelial cells after experimental ischemic stroke and hypoxia/ischemia, suggesting a potential role of astrocytic and endothelial ET-1 in ischemic brain injury. Previously, we reported that transgenic mice over-expressing ET-1 in astrocytes (GET-1 mice) displayed increased cerebral infarct size and more severe neurological deficits upon focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). However, the mechanism behind astrocytic ET-1 on ischemia-induced brain injury was not clear. Here, we report that GET mice showed lower occludin levels and increased Evans blue extravasation, suggesting increased blood-brain barrier (BBB) breakdown in GET-1 mice after MCAO. GET-1 mice also displayed increased brain swelling and brain water content together with decreased occludin and up-regulated aquaporin 4 expression. These results suggested that increased astrocytic ET-1 resulted in BBB disruption leading to increased formation of brain edema and swelling, infarct and neurological deficits and therefore imposed adverse effects on brain injury after focal cerebral ischemia. Acknowledgement: Supported by Research Grants Council and Area of Excellence from University Grants Council of Hong Kong (AoE/B-15/01).-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG-
dc.relation.ispartofNeurosignalsen_HK
dc.titleEndothelin-1 overexpression leads to blood-brain barrier disruption, more brain edema and increased aquaporin 4 expression in astrocytic processes after experimental strokeen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailFung, KL: maggie-fungkl@yahoo.comen_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.doi10.1159/000095356-
dc.identifier.hkuros106144en_HK

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