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Article: COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice

TitleCOX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice
Authors
Issue Date2003
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.com
Citation
Neuroreport, 2003, v. 14 n. 15, p. 1927-1929 How to Cite?
AbstractThe primary lesion in Parkinson's disease is the death of dopaminergic neurons in the substantia nigra.The role of cyclooxygenase (COX)-2 in the etiology of Parkinson's disease was explored using COX-2 gene knockout mice. Mortality after injection of I -methyl-4-phanyl-l,2,3,6 tetrahydropyridine (MPTP, a chemical known to cause parkinsonism in humans) in heterozygous COX-2-deficient mice was lower than that in wild-type mice. The number of tyrosine hydroxylase immunoreactive neurons in the substantia nigra pars compacta of MPTP-treated wild-type mice declined to a greater extent than in heterozygous mice. Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. This result suggested that inhibition of COX-2 has potential therapeutic implications. © 2003 Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/162752
ISSN
2015 Impact Factor: 1.343
2015 SCImago Journal Rankings: 0.783
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFeng, Zen_US
dc.contributor.authorLi, Den_US
dc.contributor.authorFung, PCWen_US
dc.contributor.authorPei, Zen_US
dc.contributor.authorRamsden, DBen_US
dc.contributor.authorHo, SLen_US
dc.date.accessioned2012-09-05T05:23:05Z-
dc.date.available2012-09-05T05:23:05Z-
dc.date.issued2003en_US
dc.identifier.citationNeuroreport, 2003, v. 14 n. 15, p. 1927-1929en_US
dc.identifier.issn0959-4965en_US
dc.identifier.urihttp://hdl.handle.net/10722/162752-
dc.description.abstractThe primary lesion in Parkinson's disease is the death of dopaminergic neurons in the substantia nigra.The role of cyclooxygenase (COX)-2 in the etiology of Parkinson's disease was explored using COX-2 gene knockout mice. Mortality after injection of I -methyl-4-phanyl-l,2,3,6 tetrahydropyridine (MPTP, a chemical known to cause parkinsonism in humans) in heterozygous COX-2-deficient mice was lower than that in wild-type mice. The number of tyrosine hydroxylase immunoreactive neurons in the substantia nigra pars compacta of MPTP-treated wild-type mice declined to a greater extent than in heterozygous mice. Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. This result suggested that inhibition of COX-2 has potential therapeutic implications. © 2003 Lippincott Williams & Wilkins.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.neuroreport.comen_US
dc.relation.ispartofNeuroReporten_US
dc.subject.mesh1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridineen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshDopamine Agents - Toxicityen_US
dc.subject.meshGenotypeen_US
dc.subject.meshIsoenzymes - Deficiency - Geneticsen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshParkinson Disease, Secondary - Chemically Induced - Pathologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Deficiency - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSubstantia Nigra - Enzymology - Pathologyen_US
dc.subject.meshTyrosine 3-Monooxygenase - Metabolismen_US
dc.titleCOX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type miceen_US
dc.typeArticleen_US
dc.identifier.emailHo, SL:slho@hku.hken_US
dc.identifier.authorityHo, SL=rp00240en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00001756-200310270-00009en_US
dc.identifier.pmid14561922-
dc.identifier.scopuseid_2-s2.0-0642339281en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0642339281&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume14en_US
dc.identifier.issue15en_US
dc.identifier.spage1927en_US
dc.identifier.epage1929en_US
dc.identifier.isiWOS:000220208500009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFeng, Z=7403442974en_US
dc.identifier.scopusauthoridLi, D=8371251400en_US
dc.identifier.scopusauthoridFung, PCW=7101613315en_US
dc.identifier.scopusauthoridPei, Z=23051646800en_US
dc.identifier.scopusauthoridRamsden, DB=7102612805en_US
dc.identifier.scopusauthoridHo, SL=25959633500en_US

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