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Article: Cyclooxygenase-1 gene knockout does not alter middle cerebral artery occlusion in a mouse stroke model

TitleCyclooxygenase-1 gene knockout does not alter middle cerebral artery occlusion in a mouse stroke model
Authors
Cheung, RTFPei, ZFeng, ZHZou, LY
KeywordsCyclooxygenase-1
Focal cerebral ischemia
Gene knockout
Infarct volume
Mice
Triphenyltetrazolium chloride
Issue Date2002
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neulet
Citation
Neuroscience Letters, 2002, v. 330 n. 1, p. 57-60 How to Cite?
DOI: http://dx.doi.org/10.1016/S0304-3940(02)00738-3
AbstractCyclooxygenase (COX) is crucial in inflammation; COX-1 is constitutional, and COX-2 is inducible. In this study, neurological function and infarct volume were evaluated at 24 h after permanent endovascular middle cerebral artery occlusion (MCAO) in both COX-1-gene knockout (homozygous or heterozygous) and wide-type mice. Similar infarct volumes and neurological deficits were seen among mice of different genotypes. There was no difference among the groups in arterial blood pressure and regional cerebral blood flow during the first 30 min of ischemia. Our results failed to confirm the harmful effect of losing COX-1 activity due to gene knockout in a permanent endovascular MCAO mouse stroke model. © 2002 Published by Elsevier Science Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162656
ISSN
0304-3940
2021 Impact Factor: 3.197
2020 SCImago Journal Rankings: 0.944
ISI Accession Number ID
WOS:000178384900015
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorCheung, RTFen_US
dc.contributor.authorPei, Zen_US
dc.contributor.authorFeng, ZHen_US
dc.contributor.authorZou, LYen_US
dc.date.accessioned2012-09-05T05:22:07Z-
dc.date.available2012-09-05T05:22:07Z-
dc.date.issued2002en_US
dc.identifier.citationNeuroscience Letters, 2002, v. 330 n. 1, p. 57-60en_US
dc.identifier.issn0304-3940en_US
dc.identifier.urihttp://hdl.handle.net/10722/162656-
dc.description.abstractCyclooxygenase (COX) is crucial in inflammation; COX-1 is constitutional, and COX-2 is inducible. In this study, neurological function and infarct volume were evaluated at 24 h after permanent endovascular middle cerebral artery occlusion (MCAO) in both COX-1-gene knockout (homozygous or heterozygous) and wide-type mice. Similar infarct volumes and neurological deficits were seen among mice of different genotypes. There was no difference among the groups in arterial blood pressure and regional cerebral blood flow during the first 30 min of ischemia. Our results failed to confirm the harmful effect of losing COX-1 activity due to gene knockout in a permanent endovascular MCAO mouse stroke model. © 2002 Published by Elsevier Science Ireland Ltd.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuleten_US
dc.relation.ispartofNeuroscience Lettersen_US
dc.rightsNeuroscience Letters. Copyright © Elsevier Ireland Ltd.-
dc.subjectCyclooxygenase-1-
dc.subjectFocal cerebral ischemia-
dc.subjectGene knockout-
dc.subjectInfarct volume-
dc.subjectMice-
dc.subjectTriphenyltetrazolium chloride-
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Geneticsen_US
dc.subject.meshCerebrovascular Circulation - Geneticsen_US
dc.subject.meshCyclooxygenase 1en_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshInfarction, Middle Cerebral Artery - Enzymology - Geneticsen_US
dc.subject.meshIsoenzymes - Deficiency - Genetics - Physiologyen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Deficiency - Genetics - Physiologyen_US
dc.subject.meshStroke - Enzymology - Geneticsen_US
dc.titleCyclooxygenase-1 gene knockout does not alter middle cerebral artery occlusion in a mouse stroke modelen_US
dc.typeArticleen_US
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_US
dc.identifier.authorityCheung, RTF=rp00434en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0304-3940(02)00738-3en_US
dc.identifier.pmid12213634-
dc.identifier.scopuseid_2-s2.0-0037072507en_US
dc.identifier.hkuros87557-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037072507&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume330en_US
dc.identifier.issue1en_US
dc.identifier.spage57en_US
dc.identifier.epage60en_US
dc.identifier.isiWOS:000178384900015-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridCheung, RTF=7202397498en_US
dc.identifier.scopusauthoridPei, Z=23051646800en_US
dc.identifier.scopusauthoridFeng, ZH=7403442974en_US
dc.identifier.scopusauthoridZou, LY=23391539300en_US
dc.identifier.issnl0304-3940-

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