Membrane estrogen receptors stimulate intracellular calcium release and progesterone synthesis in hypothalamic astrocytes.
Identifieur interne : 002623 ( Main/Exploration ); précédent : 002622; suivant : 002624Membrane estrogen receptors stimulate intracellular calcium release and progesterone synthesis in hypothalamic astrocytes.
Auteurs : John Kuo [États-Unis] ; Naheed Hamid ; Galyna Bondar ; Eric R. Prossnitz ; Paul MicevychSource :
- The Journal of neuroscience : the official journal of the Society for Neuroscience [ 1529-2401 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Astrocytes (métabolisme), Calcium (métabolisme), Calcium (physiologie), Cellules cultivées, Femelle, Hypothalamus (cytologie), Hypothalamus (métabolisme), Liquide intracellulaire (métabolisme), Membrane cellulaire (métabolisme), Membrane cellulaire (physiologie), Oestradiol (physiologie), Progestérone (biosynthèse), Rat Long-Evans, Rats, Récepteur alpha des oestrogènes (agonistes), Récepteur alpha des oestrogènes (déficit), Récepteur alpha des oestrogènes (génétique), Récepteur alpha des oestrogènes (physiologie), Signalisation du calcium (physiologie), Souris, Souris de lignée C57BL, Souris knockout.
- MESH :
- agonistes : Récepteur alpha des oestrogènes.
- biosynthèse : Progestérone.
- cytologie : Hypothalamus.
- déficit : Récepteur alpha des oestrogènes.
- génétique : Récepteur alpha des oestrogènes.
- métabolisme : Astrocytes, Calcium, Hypothalamus, Liquide intracellulaire, Membrane cellulaire.
- physiologie : Calcium, Membrane cellulaire, Oestradiol, Récepteur alpha des oestrogènes, Signalisation du calcium.
- Animaux, Cellules cultivées, Femelle, Rat Long-Evans, Rats, Souris, Souris de lignée C57BL, Souris knockout.
English descriptors
- KwdEn :
- Animals, Astrocytes (metabolism), Calcium (metabolism), Calcium (physiology), Calcium Signaling (physiology), Cell Membrane (metabolism), Cell Membrane (physiology), Cells, Cultured, Estradiol (physiology), Estrogen Receptor alpha (agonists), Estrogen Receptor alpha (deficiency), Estrogen Receptor alpha (genetics), Estrogen Receptor alpha (physiology), Female, Hypothalamus (cytology), Hypothalamus (metabolism), Intracellular Fluid (metabolism), Mice, Mice, Inbred C57BL, Mice, Knockout, Progesterone (biosynthesis), Rats, Rats, Long-Evans.
- MESH :
- chemical , agonists : Estrogen Receptor alpha.
- chemical , biosynthesis : Progesterone.
- chemical , deficiency : Estrogen Receptor alpha.
- chemical , genetics : Estrogen Receptor alpha.
- chemical , metabolism : Calcium.
- cytology : Hypothalamus.
- metabolism : Astrocytes, Cell Membrane, Hypothalamus, Intracellular Fluid.
- chemical , physiology : Calcium, Calcium Signaling, Cell Membrane, Estradiol, Estrogen Receptor alpha.
- Animals, Cells, Cultured, Female, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Rats, Long-Evans.
Abstract
In hypothalamic astrocytes obtained from adult female rats, estradiol rapidly increased free cytoplasmic calcium concentrations ([Ca(2+)](i)) that facilitate progesterone synthesis. The present study demonstrated that estradiol (1 nm) significantly and maximally stimulated progesterone synthesis within 5 min, supporting a rapid, nongenomic mechanism. The group I metabotropic glutamate receptor (mGluR1a) antagonist LY 367385 [(S)-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid] attenuated both the estradiol-induced [Ca(2+)](i) release and progesterone synthesis. To investigate membrane-associated estrogen receptors (mERs), agonists for ERα, ERβ, STX-activated protein, and GPR30 were compared. The selective ERα agonist propylpyrazole triole (PPT) and STX most closely mimicked the estradiol-induced [Ca(2+)](i) responses, where PPT was more potent but less efficacious than STX. Only high doses (100 nm) of selective ERβ agonist diarylpropionitrile (DPN) and GPR30 agonist G-1 induced estradiol-like [Ca(2+)](i) responses. With the exception of DPN (even at 100 nm), all agonists stimulated progesterone synthesis. The PPT- and STX-induced [Ca(2+)](i) release and progesterone synthesis were blocked by LY 367385. While the G-1-stimulated [Ca(2+)](i) release was blocked by LY 367385, progesterone synthesis was not. Since GPR30 was detected intracellularly but not in the membrane, we interpreted these results to suggest that G-1 could activate mGluR1a on the membrane and GPR30 on the smooth endoplasmic reticulum to release intracellular calcium. Although STX and G-1 maximally stimulated [Ca(2+)](i) release in astrocytes from estrogen receptor-α knock-out (ERKO) mice, estradiol in vivo did not stimulate progesterone synthesis in the ERKO mice. Together, these results indicate that mERα is mainly responsible for the rapid, membrane-initiated estradiol-signaling that leads to progesterone synthesis in hypothalamic astrocytes.
DOI: 10.1523/JNEUROSCI.1158-10.2010
PubMed: 20881113
Affiliations:
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Le document en format XML
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<term>Astrocytes (metabolism)</term>
<term>Calcium (metabolism)</term>
<term>Calcium (physiology)</term>
<term>Calcium Signaling (physiology)</term>
<term>Cell Membrane (metabolism)</term>
<term>Cell Membrane (physiology)</term>
<term>Cells, Cultured</term>
<term>Estradiol (physiology)</term>
<term>Estrogen Receptor alpha (agonists)</term>
<term>Estrogen Receptor alpha (deficiency)</term>
<term>Estrogen Receptor alpha (genetics)</term>
<term>Estrogen Receptor alpha (physiology)</term>
<term>Female</term>
<term>Hypothalamus (cytology)</term>
<term>Hypothalamus (metabolism)</term>
<term>Intracellular Fluid (metabolism)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Progesterone (biosynthesis)</term>
<term>Rats</term>
<term>Rats, Long-Evans</term>
</keywords>
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<term>Astrocytes (métabolisme)</term>
<term>Calcium (métabolisme)</term>
<term>Calcium (physiologie)</term>
<term>Cellules cultivées</term>
<term>Femelle</term>
<term>Hypothalamus (cytologie)</term>
<term>Hypothalamus (métabolisme)</term>
<term>Liquide intracellulaire (métabolisme)</term>
<term>Membrane cellulaire (métabolisme)</term>
<term>Membrane cellulaire (physiologie)</term>
<term>Oestradiol (physiologie)</term>
<term>Progestérone (biosynthèse)</term>
<term>Rat Long-Evans</term>
<term>Rats</term>
<term>Récepteur alpha des oestrogènes (agonistes)</term>
<term>Récepteur alpha des oestrogènes (déficit)</term>
<term>Récepteur alpha des oestrogènes (génétique)</term>
<term>Récepteur alpha des oestrogènes (physiologie)</term>
<term>Signalisation du calcium (physiologie)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
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</keywords>
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<keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Récepteur alpha des oestrogènes</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Hypothalamus</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Récepteur alpha des oestrogènes</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteur alpha des oestrogènes</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term>
<term>Cell Membrane</term>
<term>Hypothalamus</term>
<term>Intracellular Fluid</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Astrocytes</term>
<term>Calcium</term>
<term>Hypothalamus</term>
<term>Liquide intracellulaire</term>
<term>Membrane cellulaire</term>
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<term>Membrane cellulaire</term>
<term>Oestradiol</term>
<term>Récepteur alpha des oestrogènes</term>
<term>Signalisation du calcium</term>
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<term>Calcium Signaling</term>
<term>Cell Membrane</term>
<term>Estradiol</term>
<term>Estrogen Receptor alpha</term>
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<term>Female</term>
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<term>Cellules cultivées</term>
<term>Femelle</term>
<term>Rat Long-Evans</term>
<term>Rats</term>
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<front><div type="abstract" xml:lang="en">In hypothalamic astrocytes obtained from adult female rats, estradiol rapidly increased free cytoplasmic calcium concentrations ([Ca(2+)](i)) that facilitate progesterone synthesis. The present study demonstrated that estradiol (1 nm) significantly and maximally stimulated progesterone synthesis within 5 min, supporting a rapid, nongenomic mechanism. The group I metabotropic glutamate receptor (mGluR1a) antagonist LY 367385 [(S)-(+)-a-amino-4-carboxy-2-methylbenzeneacetic acid] attenuated both the estradiol-induced [Ca(2+)](i) release and progesterone synthesis. To investigate membrane-associated estrogen receptors (mERs), agonists for ERα, ERβ, STX-activated protein, and GPR30 were compared. The selective ERα agonist propylpyrazole triole (PPT) and STX most closely mimicked the estradiol-induced [Ca(2+)](i) responses, where PPT was more potent but less efficacious than STX. Only high doses (100 nm) of selective ERβ agonist diarylpropionitrile (DPN) and GPR30 agonist G-1 induced estradiol-like [Ca(2+)](i) responses. With the exception of DPN (even at 100 nm), all agonists stimulated progesterone synthesis. The PPT- and STX-induced [Ca(2+)](i) release and progesterone synthesis were blocked by LY 367385. While the G-1-stimulated [Ca(2+)](i) release was blocked by LY 367385, progesterone synthesis was not. Since GPR30 was detected intracellularly but not in the membrane, we interpreted these results to suggest that G-1 could activate mGluR1a on the membrane and GPR30 on the smooth endoplasmic reticulum to release intracellular calcium. Although STX and G-1 maximally stimulated [Ca(2+)](i) release in astrocytes from estrogen receptor-α knock-out (ERKO) mice, estradiol in vivo did not stimulate progesterone synthesis in the ERKO mice. Together, these results indicate that mERα is mainly responsible for the rapid, membrane-initiated estradiol-signaling that leads to progesterone synthesis in hypothalamic astrocytes.</div>
</front>
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<name sortKey="Hamid, Naheed" sort="Hamid, Naheed" uniqKey="Hamid N" first="Naheed" last="Hamid">Naheed Hamid</name>
<name sortKey="Micevych, Paul" sort="Micevych, Paul" uniqKey="Micevych P" first="Paul" last="Micevych">Paul Micevych</name>
<name sortKey="Prossnitz, Eric R" sort="Prossnitz, Eric R" uniqKey="Prossnitz E" first="Eric R" last="Prossnitz">Eric R. Prossnitz</name>
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<country name="États-Unis"><noRegion><name sortKey="Kuo, John" sort="Kuo, John" uniqKey="Kuo J" first="John" last="Kuo">John Kuo</name>
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