File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Human catechol-O-methyltransferase down-regulation by estradiol

TitleHuman catechol-O-methyltransferase down-regulation by estradiol
Authors
Issue Date2003
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharm
Citation
Neuropharmacology, 2003, v. 45 n. 7, p. 1011-1018 How to Cite?
AbstractCatechol-O-methyltransferase (COMT) is a crucial enzyme in dopamine and levodopa metabolism. Previously we reported that physiological concentrations of 17β-estradiol (E2) down-regulated steady-state 1.3-kb COMT mRNA levels in MCF-7 cells. In this study, we investigated whether similar reductions occurred in a glial cell line (U138MG) and whether COMT protein and activity levels paralleled the reduction in COMT mRNA levels in MCF-7 cells. In addition, we explored the mechanism of E2 action. E2 had no effect on COMT mRNA levels in U138MG cells, but significantly reduced COMT protein and activity in MCF-7 cells (activity by 53% at 10 -7 M of E2, by 45% at 10 -8 M, and by 28% at 10 -9 M relative to non-E2-treated cells). A specific estrogen receptor antagonist (ICI 182780) blocked these estrogenic effects. Estrogen receptor in nuclear extracts of MCF-7 cells, which were pretreated with E2 (10 -9 M) for 48 h, bound to the whole proximal and distal promoter regions, as determined by electrophoretic mobility shift analysis (EMSA). We propose that E2 decreased COMT activity through down-regulation of its gene and protein expression mediated via ER interaction with response elements in the promoter region of the gene. Our findings may explain the lower of COMT activity in women compared to that in men, and, in part, the beneficial effects of E2 therapy in post-menopausal Parkinson's disease patients. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162727
ISSN
2015 Impact Factor: 4.936
2015 SCImago Journal Rankings: 2.506
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Hen_US
dc.contributor.authorXie, Ten_US
dc.contributor.authorRamsden, DBen_US
dc.contributor.authorHo, SLen_US
dc.date.accessioned2012-09-05T05:22:49Z-
dc.date.available2012-09-05T05:22:49Z-
dc.date.issued2003en_US
dc.identifier.citationNeuropharmacology, 2003, v. 45 n. 7, p. 1011-1018en_US
dc.identifier.issn0028-3908en_US
dc.identifier.urihttp://hdl.handle.net/10722/162727-
dc.description.abstractCatechol-O-methyltransferase (COMT) is a crucial enzyme in dopamine and levodopa metabolism. Previously we reported that physiological concentrations of 17β-estradiol (E2) down-regulated steady-state 1.3-kb COMT mRNA levels in MCF-7 cells. In this study, we investigated whether similar reductions occurred in a glial cell line (U138MG) and whether COMT protein and activity levels paralleled the reduction in COMT mRNA levels in MCF-7 cells. In addition, we explored the mechanism of E2 action. E2 had no effect on COMT mRNA levels in U138MG cells, but significantly reduced COMT protein and activity in MCF-7 cells (activity by 53% at 10 -7 M of E2, by 45% at 10 -8 M, and by 28% at 10 -9 M relative to non-E2-treated cells). A specific estrogen receptor antagonist (ICI 182780) blocked these estrogenic effects. Estrogen receptor in nuclear extracts of MCF-7 cells, which were pretreated with E2 (10 -9 M) for 48 h, bound to the whole proximal and distal promoter regions, as determined by electrophoretic mobility shift analysis (EMSA). We propose that E2 decreased COMT activity through down-regulation of its gene and protein expression mediated via ER interaction with response elements in the promoter region of the gene. Our findings may explain the lower of COMT activity in women compared to that in men, and, in part, the beneficial effects of E2 therapy in post-menopausal Parkinson's disease patients. © 2003 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/neuropharmen_US
dc.relation.ispartofNeuropharmacologyen_US
dc.subject.meshAntibody Specificityen_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCatechol O-Methyltransferase - Biosynthesis - Genetics - Immunologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshDna - Biosynthesis - Geneticsen_US
dc.subject.meshDown-Regulation - Drug Effectsen_US
dc.subject.meshElectrophoresis, Polyacrylamide Gelen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshEstradiol - Pharmacologyen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunochemistryen_US
dc.subject.meshNuclear Proteins - Metabolismen_US
dc.subject.meshPrecipitin Testsen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshResponse Elements - Drug Effects - Geneticsen_US
dc.titleHuman catechol-O-methyltransferase down-regulation by estradiolen_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.doi10.1016/S0028-3908(03)00286-7en_US
dc.identifier.pmid14573393-
dc.identifier.scopuseid_2-s2.0-0142027141en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0142027141&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume45en_US
dc.identifier.issue7en_US
dc.identifier.spage1011en_US
dc.identifier.epage1018en_US
dc.identifier.isiWOS:000186378800013-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridJiang, H=36077295400en_US
dc.identifier.scopusauthoridXie, T=7103076362en_US
dc.identifier.scopusauthoridRamsden, DB=7102612805en_US
dc.identifier.scopusauthoridHo, SL=25959633500en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats