Membrane estrogen receptor-α-mediated nongenomic actions of phytoestrogens in GH3/B6/F10 pituitary tumor cells
Identifieur interne : 002784 ( Main/Exploration ); précédent : 002783; suivant : 002785Membrane 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>
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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>
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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>
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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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