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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:36:02Z</responseDate> <request identifier=oai:HAL:inserm-00804935v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:inserm-00804935v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:INSERM</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:HL</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-CCII</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:IRSET-1</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> <setSpec>collection:IRSET-EHESP</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Differential regulation of drug transporter expression by all-trans retinoic acid in hepatoma HepaRG cells and human hepatocytes.</title> <creator>Le Vee, Marc</creator> <creator>Jouan, Elodie</creator> <creator>Stieger, Bruno</creator> <creator>FARDEL, Olivier</creator> <contributor>Contaminants Chimiques, immunité et Inflammation ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <contributor>Division of Clinical Pharmacology and Toxicology ; University hospital of Zurich [Zurich]</contributor> <contributor>Contaminants Chimiques, immunité et Inflammation ; Service d'Hématologie, Immunologie et de Thérapie Cellulaire (HITC) ; Université de Rennes 1 (UR1) - Hôpital Pontchaillou - CHU Pontchaillou [Rennes] - Université de Rennes 1 (UR1) - Hôpital Pontchaillou - CHU Pontchaillou [Rennes] - Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor> <description>International audience</description> <source>ISSN: 0928-0987</source> <source>European Journal of Pharmaceutical Sciences</source> <publisher>Elsevier</publisher> <identifier>inserm-00804935</identifier> <identifier>http://www.hal.inserm.fr/inserm-00804935</identifier> <source>http://www.hal.inserm.fr/inserm-00804935</source> <source>European Journal of Pharmaceutical Sciences, Elsevier, 2013, 48 (4-5), pp.767-74. 〈10.1016/j.ejps.2013.01.005〉</source> <identifier>DOI : 10.1016/j.ejps.2013.01.005</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ejps.2013.01.005</relation> <identifier>PUBMED : 23352986</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/23352986</relation> <language>en</language> <subject lang=en>Regulation</subject> <subject lang=en>Hepatocytes</subject> <subject lang=en>Retinoic acid</subject> <subject lang=en>Drug transporters</subject> <subject lang=en>RXR</subject> <subject lang=en>RAR</subject> <subject>[SDV.SP] Life Sciences [q-bio]/Pharmaceutical sciences</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>All-trans retinoic acid (atRA) is the active form of vitamin A, known to activate retinoid receptors, especially the heterodimer retinoid X receptor (RXR):retinoic acid receptor (RAR) that otherwise may play a role in regulation of some drug transporters. The present study was designed to characterize the nature of human hepatic transporters that may be targeted by atRA and the heterodimer RXR:RAR. Exposure of human hepatoma HepaRG cells and primary human hepatocytes to 5μM atRA down-regulated mRNA levels of various sinusoidal solute carrier (SLC) influx transporters, including organic anion transporting polypeptide (OATP) 2B1, OATP1B1, organic cation transporter (OCT) 1 and organic anion transporter (OAT) 2, and induced those of the canalicular breast cancer resistance protein (BCRP). The retinoid concomitantly reduced protein expression of OATP2B1 and OATP1B1 and activity of OATPs and OCT1 and induced BCRP protein expression in HepaRG cells. Some transporters such as OATP1B3 and the bile salt export pump (BSEP) were however down-regulated by atRA in primary human hepatocytes, but induced in HepaRG cells, thus pointing out discrepancies between these two liver cell models in terms of detoxifying protein regulation. atRA-mediated repressions of OATP2B1, OATP1B1, OAT2 and OCT1 mRNA expression were finally shown to be counteracted by knocking-down expression of RARα and RXRα through siRNA transfection in HepaRG cells. atRA thus differentially regulated human hepatic drug transporters, mainly in a RXR:RAR-dependent manner, therefore establishing retinoids and retinoid receptors as modulators of liver drug transporter expression.</description> <date>2013-03-12</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>