High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids
Identifieur interne : 001843 ( Istex/Corpus ); précédent : 001842; suivant : 001844High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids
Auteurs : Jean Guibourdenche ; Sylvie Roulier ; Cécile Rochette-Egly ; Danièle Evain-BrionSource :
- Journal of Cellular Physiology [ 0021-9541 ] ; 1998-09.
Abstract
Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title><author><name sortKey="Guibourdenche, Jean" sort="Guibourdenche, Jean" uniqKey="Guibourdenche J" first="Jean" last="Guibourdenche">Jean Guibourdenche</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Roulier, Sylvie" sort="Roulier, Sylvie" uniqKey="Roulier S" first="Sylvie" last="Roulier">Sylvie Roulier</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Rochette Gly, Cecile" sort="Rochette Gly, Cecile" uniqKey="Rochette Gly C" first="Cécile" last="Rochette-Egly">Cécile Rochette-Egly</name><affiliation><mods:affiliation>IGBMC, BP 163, CU de Strasbourg, France</mods:affiliation></affiliation></author><author><name sortKey="Evain Rion, Daniele" sort="Evain Rion, Daniele" uniqKey="Evain Rion D" first="Danièle" last="Evain-Brion">Danièle Evain-Brion</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:111C6403133F551893FB1C5394DE2D584D80118B</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z</idno><idno type="url">https://api.istex.fr/document/111C6403133F551893FB1C5394DE2D584D80118B/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001843</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001843</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title><author><name sortKey="Guibourdenche, Jean" sort="Guibourdenche, Jean" uniqKey="Guibourdenche J" first="Jean" last="Guibourdenche">Jean Guibourdenche</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Roulier, Sylvie" sort="Roulier, Sylvie" uniqKey="Roulier S" first="Sylvie" last="Roulier">Sylvie Roulier</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Rochette Gly, Cecile" sort="Rochette Gly, Cecile" uniqKey="Rochette Gly C" first="Cécile" last="Rochette-Egly">Cécile Rochette-Egly</name><affiliation><mods:affiliation>IGBMC, BP 163, CU de Strasbourg, France</mods:affiliation></affiliation></author><author><name sortKey="Evain Rion, Daniele" sort="Evain Rion, Daniele" uniqKey="Evain Rion D" first="Danièle" last="Evain-Brion">Danièle Evain-Brion</name><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Cellular Physiology</title><title level="j" type="abbrev">J. Cell. Physiol.</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-09">1998-09</date><biblScope unit="volume">176</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="601">601</biblScope></imprint><idno type="ISSN">0021-9541</idno></series><idno type="istex">111C6403133F551893FB1C5394DE2D584D80118B</idno><idno type="DOI">10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z</idno><idno type="ArticleID">JCP16</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jean Guibourdenche</name><affiliations><json:string>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Sylvie Roulier</name><affiliations><json:string>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</json:string></affiliations></json:item><json:item><name>Cécile Rochette‐Egly</name><affiliations><json:string>IGBMC, BP 163, CU de Strasbourg, France</json:string></affiliations></json:item><json:item><name>Danièle Evain‐Brion</name><affiliations><json:string>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</json:string><json:string>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France</json:string></affiliations></json:item></author><articleId><json:string>JCP16</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.404</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1362</abstractCharCount><pdfWordCount>4692</pdfWordCount><pdfCharCount>28005</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>226</abstractWordCount></qualityIndicators><title>High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title><refBibs><json:item><author><json:item><name>R. Benveniste</name></json:item><json:item><name>K. V. 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Commun.</title></host><title>Expression of retinoic acid receptor subtypes and cellular retinoic acid binding protein‐II mRNAs during differentiation of human trophoblast cells.</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>176</volume><publisherId><json:string>JCP</json:string></publisherId><pages><total>7</total><last>601</last><first>595</first></pages><issn><json:string>0021-9541</json:string></issn><issue>3</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1097-4652</json:string></eissn><title>Journal of Cellular Physiology</title><doi><json:string>10.1002/(ISSN)1097-4652</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>physiology</json:string><json:string>cell biology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>biochemistry & molecular biology</json:string></scienceMetrix></categories><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1002/(SICI)1097-4652(199809)176:3>595::AID-JCP16>3.0.CO;2-Z</json:string></doi><id>111C6403133F551893FB1C5394DE2D584D80118B</id><score>0.18130977</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/111C6403133F551893FB1C5394DE2D584D80118B/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/111C6403133F551893FB1C5394DE2D584D80118B/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/111C6403133F551893FB1C5394DE2D584D80118B/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 1998 Wiley‐Liss, Inc.</p></availability><date>1998</date></publicationStmt><notesStmt><note>Contrat de Recherche clinique - No. 95766;</note><note>Association de Recherche sur le Cancer</note><note>La Fondation pour la Recherche Médicale</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title><author xml:id="author-1"><persName><forename type="first">Jean</forename><surname>Guibourdenche</surname></persName><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Sylvie</forename><surname>Roulier</surname></persName><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Cécile</forename><surname>Rochette‐Egly</surname></persName><affiliation>IGBMC, BP 163, CU de Strasbourg, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Danièle</forename><surname>Evain‐Brion</surname></persName><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France</affiliation></author></analytic><monogr><title level="j">Journal of Cellular Physiology</title><title level="j" type="abbrev">J. Cell. Physiol.</title><idno type="pISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><idno type="DOI">10.1002/(ISSN)1097-4652</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-09"></date><biblScope unit="volume">176</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="601">601</biblScope></imprint></monogr><idno type="istex">111C6403133F551893FB1C5394DE2D584D80118B</idno><idno type="DOI">10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z</idno><idno type="ArticleID">JCP16</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</p></abstract></profileDesc><revisionDesc><change when="1997-07-17">Received</change><change when="1998-01-20">Registration</change><change when="1998-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/111C6403133F551893FB1C5394DE2D584D80118B/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4652</doi><issn type="print">0021-9541</issn><issn type="electronic">1097-4652</issn><idGroup><id type="product" value="JCP"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR PHYSIOLOGY">Journal of Cellular Physiology</title><title type="short">J. 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It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Retinoid effects on JEG‐3 cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>High retinoid X receptor expression in JEG‐3 choriocarcinoma cells: Involvement in cell function modulation by retinoids</title></titleInfo><name type="personal"><namePart type="given">Jean</namePart><namePart type="family">Guibourdenche</namePart><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sylvie</namePart><namePart type="family">Roulier</namePart><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cécile</namePart><namePart type="family">Rochette‐Egly</namePart><affiliation>IGBMC, BP 163, CU de Strasbourg, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Danièle</namePart><namePart type="family">Evain‐Brion</namePart><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, Paris, France</affiliation><affiliation>Unité INSERM 427, Faculté des Sciences Pharmaceutiques et Biologiques de Paris, Université René Descartes, 4 Avenue de l'Observatoire, 75006 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-09</dateIssued><dateCaptured encoding="w3cdtf">1997-07-17</dateCaptured><dateValid encoding="w3cdtf">1998-01-20</dateValid><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="references">44</extent><extent unit="words">5395</extent></physicalDescription><abstract lang="en">Retinoic acid (RA) is an important mediator of cell differentiation. It stimulates hCG secretion by JEG‐3 choriocarcinoma cells in vitro after a time lag. The first aim of this study was to characterize which types of retinoid receptors (RARs and RXRs) are present in JEG‐3 cells. Using Western blot analysis and immunocytochemistry with specific antibodies as well as Northern blot analysis, we found that JEG‐3 cells expressed RARα and RXRα, the latter being the predominant receptor. We then analyzed the action on cell proliferation and hCG secretion of the physiological retinoids all‐trans RA (RA) and 9 cis RA as well as synthetic retinoids with specific affinity for RARα and RXRα. All these retinoids were potent inhibitors of cell growth, maximal inhibition (72 ± 2%) being observed after 4 days of treatment with Ro 25, a RXRα specific ligand. Within 24 h, 9 cis RA and Ro 25 stimulated hCG secretion, and maximal stimulation (1,472 ± 10%) occurred at 48 h with the RXRα‐specific ligand. The RARα‐specific ligand also stimulated hCG secretion but to a lower extend and after a delay of 48 h. These results suggest a predominant role of RXRα in mediating the biological effects of retinoids on JEG‐3 cells and the possible induction by RA itself of the metabolic pathway leading to 9 cis RA. J. Cell. Physiol. 176:595–601, 1998. © 1998 Wiley‐Liss, Inc.</abstract><note type="funding">Contrat de Recherche clinique - No. 95766; </note><note type="funding">Association de Recherche sur le Cancer</note><note type="funding">La Fondation pour la Recherche Médicale</note><relatedItem type="host"><titleInfo><title>Journal of Cellular Physiology</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. Physiol.</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0021-9541</identifier><identifier type="eISSN">1097-4652</identifier><identifier type="DOI">10.1002/(ISSN)1097-4652</identifier><identifier type="PublisherID">JCP</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>176</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>595</start><end>601</end><total>7</total></extent></part></relatedItem><identifier type="istex">111C6403133F551893FB1C5394DE2D584D80118B</identifier><identifier type="DOI">10.1002/(SICI)1097-4652(199809)176:3<595::AID-JCP16>3.0.CO;2-Z</identifier><identifier type="ArticleID">JCP16</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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