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Estrogens exert a rapid apoptotic action in anterior pituitary cells.

Identifieur interne : 001F14 ( PubMed/Checkpoint ); précédent : 001F13; suivant : 001F15

Estrogens exert a rapid apoptotic action in anterior pituitary cells.

Auteurs : S. Zárate [Argentine] ; G. Jaita ; V. Zaldivar ; D B Radl ; G. Eijo ; J. Ferraris ; D. Pisera ; A. Seilicovich

Source :

RBID : pubmed:19158323

Descripteurs français

English descriptors

Abstract

It is now accepted that estrogens not only stimulate lactotrope proliferation but also sensitize anterior pituitary cells to proapoptotic stimuli. In addition to their classical mechanism of action through binding to intracellular estrogen receptors (ERs), there is increasing evidence that estrogens exert rapid actions mediated by cell membrane-localized ERs (mERs). In the present study, we examined the involvement of membrane-initiated steroid signaling in the proapoptotic action of estradiol in primary cultures of anterior pituitary cells from ovariectomized rats by using estren, a synthetic estrogen with no effect on classical transcription and a cell-impermeable 17beta-estradiol conjugate (E2-BSA). Both compounds induced cell death of anterior pituitary cells after 60 min of incubation as assessed by flow cytometry and the [3-(4,5-dimethylthiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Estren, E2, and E2-BSA induced apoptosis of lactotropes and somatotropes as evaluated by the deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and immunodetection of prolactin (PRL) and growth hormone (GH). The proapoptotic effect of E2-BSA was abrogated by ICI-182,780, an antagonist of ERs. The expression of membrane-associated ERalpha was observed in PRL- and GH-bearing cells. Our results indicate that estradiol is able to exert a rapid apoptotic action in anterior pituitary cells, especially lactotropes and somatotropes, by a mechanism triggered by mERs. This mechanism could be involved in anterior pituitary cell turnover.

DOI: 10.1152/ajpendo.90785.2008
PubMed: 19158323


Affiliations:


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pubmed:19158323

Le document en format XML

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<term>Animals</term>
<term>Apoptosis (drug effects)</term>
<term>Cells, Cultured</term>
<term>Estradiol (pharmacology)</term>
<term>Estrenes (pharmacology)</term>
<term>Estrogens (pharmacology)</term>
<term>Female</term>
<term>Growth Hormone (metabolism)</term>
<term>Pituitary Gland, Anterior (drug effects)</term>
<term>Pituitary Gland, Anterior (metabolism)</term>
<term>Pituitary Gland, Anterior (physiology)</term>
<term>Prolactin (metabolism)</term>
<term>Rats</term>
<term>Rats, Wistar</term>
<term>Receptors, Estrogen (metabolism)</term>
<term>Time Factors</term>
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<term>Adénohypophyse ()</term>
<term>Adénohypophyse (métabolisme)</term>
<term>Adénohypophyse (physiologie)</term>
<term>Animaux</term>
<term>Apoptose ()</term>
<term>Cellules cultivées</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Hormone de croissance (métabolisme)</term>
<term>Oestradiol (pharmacologie)</term>
<term>Oestrogènes (pharmacologie)</term>
<term>Oestrènes (pharmacologie)</term>
<term>Prolactine (métabolisme)</term>
<term>Rat Wistar</term>
<term>Rats</term>
<term>Récepteurs des oestrogènes (métabolisme)</term>
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<term>Growth Hormone</term>
<term>Prolactin</term>
<term>Receptors, Estrogen</term>
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<term>Estradiol</term>
<term>Estrenes</term>
<term>Estrogens</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Apoptosis</term>
<term>Pituitary Gland, Anterior</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Pituitary Gland, Anterior</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Adénohypophyse</term>
<term>Hormone de croissance</term>
<term>Prolactine</term>
<term>Récepteurs des oestrogènes</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr">
<term>Oestradiol</term>
<term>Oestrogènes</term>
<term>Oestrènes</term>
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<term>Adénohypophyse</term>
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<term>Pituitary Gland, Anterior</term>
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<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Facteurs temps</term>
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<div type="abstract" xml:lang="en">It is now accepted that estrogens not only stimulate lactotrope proliferation but also sensitize anterior pituitary cells to proapoptotic stimuli. In addition to their classical mechanism of action through binding to intracellular estrogen receptors (ERs), there is increasing evidence that estrogens exert rapid actions mediated by cell membrane-localized ERs (mERs). In the present study, we examined the involvement of membrane-initiated steroid signaling in the proapoptotic action of estradiol in primary cultures of anterior pituitary cells from ovariectomized rats by using estren, a synthetic estrogen with no effect on classical transcription and a cell-impermeable 17beta-estradiol conjugate (E2-BSA). Both compounds induced cell death of anterior pituitary cells after 60 min of incubation as assessed by flow cytometry and the [3-(4,5-dimethylthiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Estren, E2, and E2-BSA induced apoptosis of lactotropes and somatotropes as evaluated by the deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and immunodetection of prolactin (PRL) and growth hormone (GH). The proapoptotic effect of E2-BSA was abrogated by ICI-182,780, an antagonist of ERs. The expression of membrane-associated ERalpha was observed in PRL- and GH-bearing cells. Our results indicate that estradiol is able to exert a rapid apoptotic action in anterior pituitary cells, especially lactotropes and somatotropes, by a mechanism triggered by mERs. This mechanism could be involved in anterior pituitary cell turnover.</div>
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<Title>American journal of physiology. Endocrinology and metabolism</Title>
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<AbstractText>It is now accepted that estrogens not only stimulate lactotrope proliferation but also sensitize anterior pituitary cells to proapoptotic stimuli. In addition to their classical mechanism of action through binding to intracellular estrogen receptors (ERs), there is increasing evidence that estrogens exert rapid actions mediated by cell membrane-localized ERs (mERs). In the present study, we examined the involvement of membrane-initiated steroid signaling in the proapoptotic action of estradiol in primary cultures of anterior pituitary cells from ovariectomized rats by using estren, a synthetic estrogen with no effect on classical transcription and a cell-impermeable 17beta-estradiol conjugate (E2-BSA). Both compounds induced cell death of anterior pituitary cells after 60 min of incubation as assessed by flow cytometry and the [3-(4,5-dimethylthiazol-2-yl)]-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Estren, E2, and E2-BSA induced apoptosis of lactotropes and somatotropes as evaluated by the deoxynucleotidyltransferase-mediated dUTP nick end-labeling assay and immunodetection of prolactin (PRL) and growth hormone (GH). The proapoptotic effect of E2-BSA was abrogated by ICI-182,780, an antagonist of ERs. The expression of membrane-associated ERalpha was observed in PRL- and GH-bearing cells. Our results indicate that estradiol is able to exert a rapid apoptotic action in anterior pituitary cells, especially lactotropes and somatotropes, by a mechanism triggered by mERs. This mechanism could be involved in anterior pituitary cell turnover.</AbstractText>
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<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C468666">4-estren-3,17-diol</NameOfSubstance>
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<Chemical>
<RegistryNumber>0</RegistryNumber>
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<MeshHeading>
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