| Estrogen- and xenoestrogen-induced ERK signaling in pituitary tumor cells involves estrogen receptor-α interactions with G protein-αi and caveolin I. | |
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MedLine Citation:
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PMID: 22230296 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Multiple physiologic estrogens (estradiol, estriol, and estrone), as well as xenoestrogenic compounds (including alkylphenols and bisphenol A), can act via nongenomic signaling initiated by liganding of the plasma membrane estrogen receptor-α (mERα). We examined heterotrimeric G protein involvement leading to extracellular-regulated kinase (ERK) activation in GH3/B6/F10 rat anterior pituitary tumor cells that express abundant mERα, and smaller amounts of mERβ and GPR30. A combination of microarrays, immunoblots, and quantitative immunoassays demonstrated the expression of members of all α, β, and γ G protein classes in these cells. Use of selective inhibitors showed that the G(αi) subtype was the primary initiator of downstream ERK signaling. Using antibodies against the GTP-bound form of G(α) protein subtypes i and s, we showed that xenoestrogens (bisphenol A, nonylphenol) activated G(αi) at 15-30s; all alkylphenols examined subsequently suppressed activation by 5min. GTP-activation of G(αi) for all estrogens was enhanced by irreversible cumulative binding to GTPγS. In contrast, G(αs) was neither activated nor deactivated by these treatments with estrogens. ERα and G(αi) co-localized outside nuclei and could be immuno-captured together. Interactions of ERα with G(αi) and caveolin I were demonstrated by epitope proximity ligation assays. An ERα/β antagonist (ICI182780) and a selective disruptor of caveolar structures (nystatin) blocked estrogen-induced ERK activation. Conclusions: Xenoestrogens, like physiologic estrogens, can evoke downstream kinase signaling involving selective interactions of ERα with G(αi) and caveolin I, but with some different characteristics, which could explain their disruptive actions. |
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Authors:
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Cheryl S Watson; Yow-Jiun Jeng; Guangzhen Hu; Ann Wozniak; Nataliya Bulayeva; Jutatip Guptarak |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-12-30 |
Journal Detail:
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Title: Steroids Volume: 77 ISSN: 1878-5867 ISO Abbreviation: Steroids Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-03-14 Completed Date: 2012-08-14 Revised Date: 2013-04-03 |
Medline Journal Info:
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Nlm Unique ID: 0404536 Medline TA: Steroids Country: United States |
Other Details:
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Languages: eng Pagination: 424-32 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Dept. of Biochemistry & Molecular Biology, Univ. of Texas Medical Branch, Galveston, TX 77555-0645, USA. cswatson@utmb.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Caveolae / metabolism Caveolin 1 / genetics, metabolism* Cell Line, Tumor Cell Membrane / metabolism Estrogen Receptor alpha / genetics, metabolism* Estrogens / pharmacology* Estrogens, Non-Steroidal / pharmacology Extracellular Signal-Regulated MAP Kinases / metabolism GTP-Binding Protein alpha Subunits, Gi-Go / genetics, metabolism* Guanosine Triphosphate / metabolism Immunoblotting MAP Kinase Signaling System / drug effects* Microscopy, Fluorescence Oligonucleotide Array Sequence Analysis Phenols / pharmacology* Pituitary Neoplasms / genetics, metabolism, pathology Protein Binding / drug effects Rats |
| Grant Support | |
ID/Acronym/Agency:
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R01 ES015292/ES/NIEHS NIH HHS; R01 ES015292-03/ES/NIEHS NIH HHS; R01 ES015292-04/ES/NIEHS NIH HHS; R01 ES015292-04S1/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Caveolin 1; 0/Estrogen Receptor alpha; 0/Estrogens; 0/Estrogens, Non-Steroidal; 0/Phenols; 25154-52-3/nonylphenol; 86-01-1/Guanosine Triphosphate; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.1/GTP-Binding Protein alpha Subunits, Gi-Go; MLT3645I99/bisphenol A |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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