Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH3/B6/F10 pituitary tumor cells
Identifieur interne : 001375 ( Pmc/Checkpoint ); précédent : 001374; suivant : 001376Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH3/B6/F10 pituitary tumor cells
Auteurs : Yow-Jiun Jeng [États-Unis] ; Mikhail Y. Kochukov [États-Unis] ; Cheryl S. Watson [États-Unis]Source :
- Journal of Molecular Signaling [ 1750-2187 ] ; 2009.
Abstract
Estradiol (E2) mediates various intracellular signaling cascades from the plasma membrane via several estrogen receptors (ERs). The pituitary is an estrogen-responsive tissue, and we have previously reported that E2 can activate mitogen-activated protein kinases (MAPKs) such as ERK1/2 and JNK1/2/3 in the membrane ERα (mERα)-enriched GH3/B6/F10 rat pituitary tumor cell line. Phytoestrogens are compounds found in plants and foods such as soybeans, alfalfa sprouts, and red grapes. They are structurally similar to E2 and share a similar mechanism of action through their binding to ERs. Phytoestrogens bind to nuclear ERs with a much lower affinity and therefore are less potent in mediating genomic responses. However, little is known about their ability to act via mERs to mediate nongenomic effects.
To investigate the activation of different nongenomic pathways, and determine the involvement of mERα, we measured prolactin (PRL) release by radio-immunoassay, MAPK activations (ERK1/2 and JNK1/2/3) via a quantitative plate immunoassay, and intracellular [Ca2+] by Fura-2 fluorescence imaging in cells treated with E2 or four different phytoestrogens (coumestrol, daidzein, genistein, and
Coumesterol and daidzein increased PRL release similar to E2 in GH3/B6/F10 cells, while genistein and
Phytoestrogens were much more potent in mediating these nongenomic responses (activation of MAPKs, PRL release, and increased intracellular [Ca2+]) via mERα than was previously reported for genomic responses. The unique non-monotonic dose responses and variant signaling patterns caused by E2 and all tested phytoestrogens suggest that complex and multiple signaling pathways or binding partners could be involved. By activating these different nongenomic signaling pathways, phytoestrogens could have significant physiological consequences for pituitary cell functions.
Url:
DOI: 10.1186/1750-2187-4-2
PubMed: 19400946
PubMed Central: 2679742
Affiliations:
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/B<sub>6</sub>
/F<sub>10 </sub>
pituitary tumor cells</title>
<author><name sortKey="Jeng, Yow Jiun" sort="Jeng, Yow Jiun" uniqKey="Jeng Y" first="Yow-Jiun" last="Jeng">Yow-Jiun Jeng</name>
<affiliation wicri:level="2"><nlm:aff id="I1">Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
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<author><name sortKey="Kochukov, Mikhail Y" sort="Kochukov, Mikhail Y" uniqKey="Kochukov M" first="Mikhail Y" last="Kochukov">Mikhail Y. Kochukov</name>
<affiliation wicri:level="2"><nlm:aff id="I1">Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</nlm:aff>
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<wicri:regionArea>Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea>
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<author><name sortKey="Watson, Cheryl S" sort="Watson, Cheryl S" uniqKey="Watson C" first="Cheryl S" last="Watson">Cheryl S. Watson</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
pituitary tumor cells</title>
<author><name sortKey="Jeng, Yow Jiun" sort="Jeng, Yow Jiun" uniqKey="Jeng Y" first="Yow-Jiun" last="Jeng">Yow-Jiun Jeng</name>
<affiliation wicri:level="2"><nlm:aff id="I1">Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
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<author><name sortKey="Kochukov, Mikhail Y" sort="Kochukov, Mikhail Y" uniqKey="Kochukov M" first="Mikhail Y" last="Kochukov">Mikhail Y. Kochukov</name>
<affiliation wicri:level="2"><nlm:aff id="I1">Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
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<author><name sortKey="Watson, Cheryl S" sort="Watson, Cheryl S" uniqKey="Watson C" first="Cheryl S" last="Watson">Cheryl S. Watson</name>
<affiliation wicri:level="2"><nlm:aff id="I1">Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
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<series><title level="j">Journal of Molecular Signaling</title>
<idno type="eISSN">1750-2187</idno>
<imprint><date when="2009">2009</date>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Estradiol (E<sub>2</sub>
) mediates various intracellular signaling cascades from the plasma membrane via several estrogen receptors (ERs). The pituitary is an estrogen-responsive tissue, and we have previously reported that E<sub>2 </sub>
can activate mitogen-activated protein kinases (MAPKs) such as ERK1/2 and JNK1/2/3 in the membrane ERα (mERα)-enriched GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
rat pituitary tumor cell line. Phytoestrogens are compounds found in plants and foods such as soybeans, alfalfa sprouts, and red grapes. They are structurally similar to E<sub>2 </sub>
and share a similar mechanism of action through their binding to ERs. Phytoestrogens bind to nuclear ERs with a much lower affinity and therefore are less potent in mediating genomic responses. However, little is known about their ability to act via mERs to mediate nongenomic effects.</p>
</sec>
<sec sec-type="methods"><title>Methods</title>
<p>To investigate the activation of different nongenomic pathways, and determine the involvement of mERα, we measured prolactin (PRL) release by radio-immunoassay, MAPK activations (ERK1/2 and JNK1/2/3) via a quantitative plate immunoassay, and intracellular [Ca<sup>2+</sup>
] by Fura-2 fluorescence imaging in cells treated with E<sub>2 </sub>
or four different phytoestrogens (coumestrol, daidzein, genistein, and <italic>trans</italic>
-resveratrol).</p>
</sec>
<sec><title>Results</title>
<p>Coumesterol and daidzein increased PRL release similar to E<sub>2 </sub>
in GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
cells, while genistein and <italic>trans</italic>
-resveratrol had no effect. All of these compounds except genistein activated ERK1/2 signaling at 1–10 picomolar concentrations; JNK 1/2/3 was activated by all compounds at a 100 nanomolar concentration. All compounds also caused rapid Ca<sup>2+ </sup>
uptake, though in unique dose-dependent Ca<sup>2+ </sup>
response patterns for several aspects of this response. A subclone of GH<sub>3 </sub>
cells expressing low levels of mERα (GH<sub>3</sub>
/B<sub>6</sub>
/D<sub>9</sub>
) did not respond to any phytoestrogen treatments for any of these responses, suggesting that these nongenomic effects were mediated via mERα.</p>
</sec>
<sec><title>Conclusion</title>
<p>Phytoestrogens were much more potent in mediating these nongenomic responses (activation of MAPKs, PRL release, and increased intracellular [Ca<sup>2+</sup>
]) via mERα than was previously reported for genomic responses. The unique non-monotonic dose responses and variant signaling patterns caused by E<sub>2 </sub>
and all tested phytoestrogens suggest that complex and multiple signaling pathways or binding partners could be involved. By activating these different nongenomic signaling pathways, phytoestrogens could have significant physiological consequences for pituitary cell functions.</p>
</sec>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Mol Signal</journal-id>
<journal-title>Journal of Molecular Signaling</journal-title>
<issn pub-type="epub">1750-2187</issn>
<publisher><publisher-name>BioMed Central</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">19400946</article-id>
<article-id pub-id-type="pmc">2679742</article-id>
<article-id pub-id-type="publisher-id">1750-2187-4-2</article-id>
<article-id pub-id-type="doi">10.1186/1750-2187-4-2</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Short Report</subject>
</subj-group>
</article-categories>
<title-group><article-title>Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
pituitary tumor cells</article-title>
</title-group>
<contrib-group><contrib id="A1" contrib-type="author"><name><surname>Jeng</surname>
<given-names>Yow-Jiun</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>yjeng@utmb.edu</email>
</contrib>
<contrib id="A2" contrib-type="author"><name><surname>Kochukov</surname>
<given-names>Mikhail Y</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>mykochuk@utmb.edu</email>
</contrib>
<contrib id="A3" corresp="yes" contrib-type="author"><name><surname>Watson</surname>
<given-names>Cheryl S</given-names>
</name>
<xref ref-type="aff" rid="I1">1</xref>
<email>cswatson@utmb.edu</email>
</contrib>
</contrib-group>
<aff id="I1"><label>1</label>
Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA</aff>
<pub-date pub-type="collection"><year>2009</year>
</pub-date>
<pub-date pub-type="epub"><day>28</day>
<month>4</month>
<year>2009</year>
</pub-date>
<volume>4</volume>
<fpage>2</fpage>
<lpage>2</lpage>
<ext-link ext-link-type="uri" xlink:href="http://www.jmolecularsignaling.com/content/4/1/2"></ext-link>
<history><date date-type="received"><day>17</day>
<month>1</month>
<year>2009</year>
</date>
<date date-type="accepted"><day>28</day>
<month>4</month>
<year>2009</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2009 Jeng et al; licensee BioMed Central Ltd.</copyright-statement>
<copyright-year>2009</copyright-year>
<copyright-holder>Jeng et al; licensee BioMed Central Ltd.</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.0"><p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/2.0"></ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
<pmc-comment>
Jeng
Yow-Jiun
yjeng@utmb.edu
Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH3/B6/F10 pituitary tumor cells
2009 Journal of Molecular Signaling 4(1): 2-. (2009) 1750-2187(2009)4:1<2> urn:ISSN:1750-2187 </pmc-comment>
</license>
</permissions>
<abstract><sec><title>Background</title>
<p>Estradiol (E<sub>2</sub>
) mediates various intracellular signaling cascades from the plasma membrane via several estrogen receptors (ERs). The pituitary is an estrogen-responsive tissue, and we have previously reported that E<sub>2 </sub>
can activate mitogen-activated protein kinases (MAPKs) such as ERK1/2 and JNK1/2/3 in the membrane ERα (mERα)-enriched GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
rat pituitary tumor cell line. Phytoestrogens are compounds found in plants and foods such as soybeans, alfalfa sprouts, and red grapes. They are structurally similar to E<sub>2 </sub>
and share a similar mechanism of action through their binding to ERs. Phytoestrogens bind to nuclear ERs with a much lower affinity and therefore are less potent in mediating genomic responses. However, little is known about their ability to act via mERs to mediate nongenomic effects.</p>
</sec>
<sec sec-type="methods"><title>Methods</title>
<p>To investigate the activation of different nongenomic pathways, and determine the involvement of mERα, we measured prolactin (PRL) release by radio-immunoassay, MAPK activations (ERK1/2 and JNK1/2/3) via a quantitative plate immunoassay, and intracellular [Ca<sup>2+</sup>
] by Fura-2 fluorescence imaging in cells treated with E<sub>2 </sub>
or four different phytoestrogens (coumestrol, daidzein, genistein, and <italic>trans</italic>
-resveratrol).</p>
</sec>
<sec><title>Results</title>
<p>Coumesterol and daidzein increased PRL release similar to E<sub>2 </sub>
in GH<sub>3</sub>
/B<sub>6</sub>
/F<sub>10 </sub>
cells, while genistein and <italic>trans</italic>
-resveratrol had no effect. All of these compounds except genistein activated ERK1/2 signaling at 1–10 picomolar concentrations; JNK 1/2/3 was activated by all compounds at a 100 nanomolar concentration. All compounds also caused rapid Ca<sup>2+ </sup>
uptake, though in unique dose-dependent Ca<sup>2+ </sup>
response patterns for several aspects of this response. A subclone of GH<sub>3 </sub>
cells expressing low levels of mERα (GH<sub>3</sub>
/B<sub>6</sub>
/D<sub>9</sub>
) did not respond to any phytoestrogen treatments for any of these responses, suggesting that these nongenomic effects were mediated via mERα.</p>
</sec>
<sec><title>Conclusion</title>
<p>Phytoestrogens were much more potent in mediating these nongenomic responses (activation of MAPKs, PRL release, and increased intracellular [Ca<sup>2+</sup>
]) via mERα than was previously reported for genomic responses. The unique non-monotonic dose responses and variant signaling patterns caused by E<sub>2 </sub>
and all tested phytoestrogens suggest that complex and multiple signaling pathways or binding partners could be involved. By activating these different nongenomic signaling pathways, phytoestrogens could have significant physiological consequences for pituitary cell functions.</p>
</sec>
</abstract>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Texas</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Texas"><name sortKey="Jeng, Yow Jiun" sort="Jeng, Yow Jiun" uniqKey="Jeng Y" first="Yow-Jiun" last="Jeng">Yow-Jiun Jeng</name>
</region>
<name sortKey="Kochukov, Mikhail Y" sort="Kochukov, Mikhail Y" uniqKey="Kochukov M" first="Mikhail Y" last="Kochukov">Mikhail Y. Kochukov</name>
<name sortKey="Watson, Cheryl S" sort="Watson, Cheryl S" uniqKey="Watson C" first="Cheryl S" last="Watson">Cheryl S. Watson</name>
</country>
</tree>
</affiliations>
</record>
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