File Download

There are no files associated with this item.

Supplementary

Conference Paper: Transgenic mice overexpressing endothelin-1 in astrocytes display greater infarct size and more severe neurological deficit after transient focal cerebral ischemia

TitleTransgenic mice overexpressing endothelin-1 in astrocytes display greater infarct size and more severe neurological deficit after transient focal cerebral ischemia
Authors
Keywordsstroke
injury
cerebral blood flow
reperfusion
Issue Date2000
PublisherSociety for Neuroscience
Citation
Neuroscience 2000, New Orleans, LA, 4-9 November 2000, Presentation no. 767.5 How to Cite?
AbstractOur preliminary studies demonstrated that endothelin-1 (ET-1) mRNA expression is increased in astrocyte-like and endothelial cells in experimentally induced hypoxia/ischemia. Therefore, we developed a transgenic mouse model to study the role of astrocytic ET-1 in cerebral injury by microinjection of a modified GFAP genomic cassette containing the mouse ET-1 cDNA. A total of 5 lines were generated. All embryos appeared to develop to full term since the number of animals being born followed Mendelian distribution. Two lines of mice, 3804 and 3808, show brain-specific transgene expression as revealed by both rt-PCR and Northern analyses. In line 3804, the brain ET-1 peptide level was increased by two folds. No obvious abnormalities were observed in the gross anatomy of the brain and cerebrovasculature of these transgenic mice. GFAP ICC also revealed no differences in the number of positively-stained astrocytes and their cellular distribution. Therefore, it appears that over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain. However, upon focal cerebral ischemia induced by transient filament occlusion of the middle cerebral artery, transgenic mouse brains displayed an increase in infarct area and infarct volume percentages. A higher number of transgenic mice showed more severe neurological deficit when compared to their wildtype littermates. The present data suggested that overexpression of ET-1 in astrocytes may have adverse effects on the brain during cerebral ischemic injury. Supported by Research Grants Council Hong Kong
Persistent Identifierhttp://hdl.handle.net/10722/108772

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorHo, MCYen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-26T00:53:47Z-
dc.date.available2010-09-26T00:53:47Z-
dc.date.issued2000en_HK
dc.identifier.citationNeuroscience 2000, New Orleans, LA, 4-9 November 2000, Presentation no. 767.5en_HK
dc.identifier.urihttp://hdl.handle.net/10722/108772-
dc.description.abstractOur preliminary studies demonstrated that endothelin-1 (ET-1) mRNA expression is increased in astrocyte-like and endothelial cells in experimentally induced hypoxia/ischemia. Therefore, we developed a transgenic mouse model to study the role of astrocytic ET-1 in cerebral injury by microinjection of a modified GFAP genomic cassette containing the mouse ET-1 cDNA. A total of 5 lines were generated. All embryos appeared to develop to full term since the number of animals being born followed Mendelian distribution. Two lines of mice, 3804 and 3808, show brain-specific transgene expression as revealed by both rt-PCR and Northern analyses. In line 3804, the brain ET-1 peptide level was increased by two folds. No obvious abnormalities were observed in the gross anatomy of the brain and cerebrovasculature of these transgenic mice. GFAP ICC also revealed no differences in the number of positively-stained astrocytes and their cellular distribution. Therefore, it appears that over-expression of ET-1 in the brain did not affect the development of the mouse embryo and the brain. However, upon focal cerebral ischemia induced by transient filament occlusion of the middle cerebral artery, transgenic mouse brains displayed an increase in infarct area and infarct volume percentages. A higher number of transgenic mice showed more severe neurological deficit when compared to their wildtype littermates. The present data suggested that overexpression of ET-1 in astrocytes may have adverse effects on the brain during cerebral ischemic injury. Supported by Research Grants Council Hong Kong-
dc.languageengen_HK
dc.publisherSociety for Neuroscience-
dc.relation.ispartofSoceity for Neuroscience Annual Meetingen_HK
dc.subjectstroke-
dc.subjectinjury-
dc.subjectcerebral blood flow-
dc.subjectreperfusion-
dc.titleTransgenic mice overexpressing endothelin-1 in astrocytes display greater infarct size and more severe neurological deficit after transient focal cerebral ischemiaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLo, ACY: amylo@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.hkuros60043en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats