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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>2018-01-15T18:40:48Z</responseDate> <request identifier=oai:HAL:hal-00682486v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-00682486v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:HL</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IRSET-CCII</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:USPC</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>MAPK- and PKC/CREB-dependent induction of interleukin-11 by the environmental contaminant formaldehyde in human bronchial epithelial cells.</title> <creator>Lecureur, Valérie</creator> <creator>Arzel, Matthieu</creator> <creator>Ameziane, Sarah</creator> <creator>Houlbert, Noémie</creator> <creator>Le Vee, Marc</creator> <creator>Jouneau, Stéphane</creator> <creator>Fardel, Olivier</creator> <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>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>Service de pneumologie</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: 0300-483X</source> <source>Toxicology</source> <publisher>Elsevier</publisher> <identifier>hal-00682486</identifier> <identifier>https://hal.archives-ouvertes.fr/hal-00682486</identifier> <source>https://hal.archives-ouvertes.fr/hal-00682486</source> <source>Toxicology, Elsevier, 2012, 292 (1), pp.13-22. 〈10.1016/j.tox.2011.11.011〉</source> <identifier>DOI : 10.1016/j.tox.2011.11.011</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.tox.2011.11.011</relation> <identifier>PUBMED : 22138297</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/22138297</relation> <language>en</language> <subject lang=en>CREB</subject> <subject lang=en>Lung epithelial cells</subject> <subject lang=en>Formaldehyde</subject> <subject lang=en>Interleukin-11</subject> <subject lang=en>MAPK</subject> <subject>[SDV.TOX] Life Sciences [q-bio]/Toxicology</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Formaldehyde (FA) is a volatile organic compound (VOC), considered as a major indoor air pollutant and suspected to favor the development of inflammatory lung diseases. The present study was aimed at identifying cytokines/chemokines targeted by FA in human lung cells. This VOC was demonstrated to up-regulate interleukin-11 (IL-11) mRNA and secretion levels in a dose-dependent manner in cultured lung epithelial BEAS-2B cells. It concomitantly induced mRNA expression of transforming growth factor (TGF)-β1, a fibrogenic marker regulated by IL-11. FA was also found to trigger an early phosphorylation of p38 and extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein kinases (MAPKs) in BEAS-2B cells, whose inhibition by ERK and p38 MAPK chemical inhibitors (U0126 and SB203580, respectively) counteracted FA-mediated induction of IL-11. In addition, FA increased phosphorylation of cAMP response element binding protein (CREB) and the use of small-interfering RNA targeting CREB demonstrated that this transcription factor was required for the up-regulation of IL-11 by FA. Implication of protein kinase C (PKC) in FA-induced IL-11 expression was moreover demonstrated by using RO-31-8220, a PKC inhibitor. We finally showed using SB203580 and RO-31-8220 that phosphorylation of CREB and CREB-promoter activity induced by FA are under the control of both p38 MAPK and PKC. Taken together, the results showed that FA uses different pathways to induce IL-11 expression in lung BEAS-2B cells. IL-11, well-known to contribute to lung inflammatory diseases, appears thus as a molecular target of FA, which could be involved in putative deleterious inflammatory and fibrogenic pulmonary effects of this VOC.</description> <date>2012-02-06</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>