| Varied mechanisms of oestradiol-mediated regulation of dopamine β-hydroxylase transcription. | |
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MedLine Citation:
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PMID: 21062376 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Experiments performed in vivo and in cell culture have demonstrated that oestradiol induces dopamine β-hydroxylase (DBH) gene transcription. In the present study, we examined oestrogen-responsive elements of the rat DBH gene promoter aiming to characterise the mechanisms of oestradiol-induced DBH transcription. Various mutations and deletions of DBH promoter reporter constructs were tested for responsiveness to 17β-oestradiol (E(2) ). Mutation of the half palindromic oestrogen response element (ERE) at position -759 reduced the response to E(2) in PC12 cells co-transfected with oestrogen receptor (ER) α, indicating a functional role for this motif. In cells co-transfected with ERβ, mutations at the -759 site were unresponsive to E(2) . To characterise the additional E(2) responsive elements, mediated by ERα, the DBH promoter was truncated to the proximal 249 or 200 nucleotides upstream of the transcription start site. Despite either truncation, 10 nm E(2) still elicited an approximately two-fold induction of DBH promoter activity. Mutation of a possible ERE-like sequence at -59 had no effect. The lack of a functional ERE in the proximal region of the rat DBH promoter despite E(2) -mediated DBH promoter activity, suggests regulation by a nonclassical mechanism, such as a membrane-initiated signalling pathway. Moreover, the induction of DBH promoter activity and the rise in DBH mRNA levels were observed within hours. To determine whether membrane-initiated E(2) signalling is involved in rat DBH gene transcription, a membrane impermeable E(2) conjugate, β-oestradiol-6-(O-carboxy-methyl) oxime-bovine serum albumin (E(2) BSA), was used. Incubation with E(2) -BSA induced luciferase activity and elicited a significant rise in DBH mRNA levels in the ERα transfected cells. The findings indicate two different mechanisms whereby DBH transcription is regulated by E(2) in the presence of ERα. The results implicate both genomic and membrane-initiated mechanisms, mediated by ERα, in E(2) -induced DBH gene transcription. |
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Authors:
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L I Serova; R Nostramo; M Veerasirikul; D B Cappell; E L Sabban |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neuroendocrinology Volume: 23 ISSN: 1365-2826 ISO Abbreviation: J. Neuroendocrinol. Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-01-11 Completed Date: 2011-05-05 Revised Date: 2012-02-02 |
Medline Journal Info:
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Nlm Unique ID: 8913461 Medline TA: J Neuroendocrinol Country: England |
Other Details:
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Languages: eng Pagination: 168-76 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors. Journal of Neuroendocrinology © 2011 Blackwell Publishing Ltd. |
Affiliation:
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Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Dopamine beta-Hydroxylase / biosynthesis*, genetics Estradiol / analogs & derivatives, pharmacology* Estrogen Receptor alpha / genetics Estrogen Receptor beta / genetics PC12 Cells Promoter Regions, Genetic Rats Response Elements / drug effects Serum Albumin, Bovine / pharmacology Signal Transduction / drug effects, genetics Transcription, Genetic / drug effects* Transfection |
| Grant Support | |
ID/Acronym/Agency:
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NS28869/NS/NINDS NIH HHS; R01 NS028869-14/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/Serum Albumin, Bovine; 35048-47-6/estradiol-6-(O-carboxymethyl)oxime; 50-28-2/Estradiol; EC 1.14.17.1/Dopamine beta-Hydroxylase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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