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Article: Interaction between inducible nitric oxide synthase and cyclooxygenase- 2 after cerebral ischemia

TitleInteraction between inducible nitric oxide synthase and cyclooxygenase- 2 after cerebral ischemia
Authors
Issue Date1998
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 1998, v. 95 n. 18, p. 10966-10971 How to Cite?
AbstractFocal cerebral ischemia is associated with expression of both inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), enzymes whose reaction products contribute to the evolution of ischemic brain injury. We tested the hypothesis that, after cerebral ischemia, nitric oxide (NO) produced by iNOS enhances COX-2 activity, thereby increasing the toxic potential of this enzyme. Cerebral ischemia was produced by middle cerebral artery occlusion in rats or mice. Twenty-four hours after ischemia in rats, iNOS-immunoreactive neutrophils were observed in close proximity (<20 μm) to COX-2-positive cells at the periphery of the infarct. In the olfactory bulb, only COX-2 positive cells were observed. Cerebral ischemia increased the concentration of the COX-2 reaction product prostaglandin E 2 (PGE 2) in the ischemic area and in the ipsilateral olfactory bulb. The iNOS inhibitor aminoguanidine reduced PGE 2 concentration in the infarct, where both iNOS and COX-2 were expressed, but not in the olfactory bulb, where only COX-2 was expressed. Postischemic PGE 2 accumulation was reduced significantly in iNOS null mice compared with wild-type controls (C57BL/6 or SV129). The data provide evidence that NO produced by iNOS influences COX-2 activity after focal cerebral ischemia. Proinflammatory prostanoids and reactive oxygen species produced by COX-2 may be a previously unrecognized factor by which NO contributes to ischemic brain injury. The pathogenic effect of the interaction between NO, or a derived specie, and COX-2 is likely to play a role also in other brain diseases associated with inflammation.
Persistent Identifierhttp://hdl.handle.net/10722/174762
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNogawa, Sen_US
dc.contributor.authorForster, Cen_US
dc.contributor.authorZhang, Fen_US
dc.contributor.authorNagayama, Men_US
dc.contributor.authorRoss, MEen_US
dc.contributor.authorIadecola, Cen_US
dc.date.accessioned2012-11-26T08:47:18Z-
dc.date.available2012-11-26T08:47:18Z-
dc.date.issued1998en_US
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 1998, v. 95 n. 18, p. 10966-10971en_US
dc.identifier.issn0027-8424en_US
dc.identifier.urihttp://hdl.handle.net/10722/174762-
dc.description.abstractFocal cerebral ischemia is associated with expression of both inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), enzymes whose reaction products contribute to the evolution of ischemic brain injury. We tested the hypothesis that, after cerebral ischemia, nitric oxide (NO) produced by iNOS enhances COX-2 activity, thereby increasing the toxic potential of this enzyme. Cerebral ischemia was produced by middle cerebral artery occlusion in rats or mice. Twenty-four hours after ischemia in rats, iNOS-immunoreactive neutrophils were observed in close proximity (<20 μm) to COX-2-positive cells at the periphery of the infarct. In the olfactory bulb, only COX-2 positive cells were observed. Cerebral ischemia increased the concentration of the COX-2 reaction product prostaglandin E 2 (PGE 2) in the ischemic area and in the ipsilateral olfactory bulb. The iNOS inhibitor aminoguanidine reduced PGE 2 concentration in the infarct, where both iNOS and COX-2 were expressed, but not in the olfactory bulb, where only COX-2 was expressed. Postischemic PGE 2 accumulation was reduced significantly in iNOS null mice compared with wild-type controls (C57BL/6 or SV129). The data provide evidence that NO produced by iNOS influences COX-2 activity after focal cerebral ischemia. Proinflammatory prostanoids and reactive oxygen species produced by COX-2 may be a previously unrecognized factor by which NO contributes to ischemic brain injury. The pathogenic effect of the interaction between NO, or a derived specie, and COX-2 is likely to play a role also in other brain diseases associated with inflammation.en_US
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_US
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBrain - Enzymology - Metabolismen_US
dc.subject.meshBrain Ischemia - Enzymology - Metabolismen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshDna Primersen_US
dc.subject.meshDinoprostone - Metabolismen_US
dc.subject.meshIsoenzymes - Genetics - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshNitric Oxide Synthase - Genetics - Metabolismen_US
dc.subject.meshNitric Oxide Synthase Type Iien_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Genetics - Metabolismen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleInteraction between inducible nitric oxide synthase and cyclooxygenase- 2 after cerebral ischemiaen_US
dc.typeArticleen_US
dc.identifier.emailZhang, F: fuchun@hkucc.hku.hken_US
dc.identifier.authorityZhang, F=rp00840en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.95.18.10966en_US
dc.identifier.pmid9724813-
dc.identifier.scopuseid_2-s2.0-0032167857en_US
dc.identifier.volume95en_US
dc.identifier.issue18en_US
dc.identifier.spage10966en_US
dc.identifier.epage10971en_US
dc.identifier.isiWOS:000075730500111-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNogawa, S=7003524387en_US
dc.identifier.scopusauthoridForster, C=36828983300en_US
dc.identifier.scopusauthoridZhang, F=14012468800en_US
dc.identifier.scopusauthoridNagayama, M=7101904077en_US
dc.identifier.scopusauthoridRoss, ME=7403661996en_US
dc.identifier.scopusauthoridIadecola, C=7006626243en_US

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