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<title lang=en>Enniatin B-induced cell death and inflammatory responses in RAW 267.4 murine macrophages.</title>
<creator>Gammelsrud, A.</creator>
<creator>Solhaug, A.</creator>
<creator>Dendelé, Béatrice</creator>
<creator>Sandberg, W. J.</creator>
<creator>IVANOVA, L.</creator>
<creator>Kocbach Bølling, A.</creator>
<creator>Lagadic-Gossmann, Dominique</creator>
<creator>Refsnes, M.</creator>
<creator>Becher, R.</creator>
<creator>Eriksen, G.</creator>
<creator>Holme, J. A.</creator>
<contributor>Division of Environmental Medicine ; Norwegian Institute of Public Health</contributor>
<contributor>Department of Chemistry and Toxicology ; Norwegian Veterinary Institute</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>Stress, membrane, signalisation ; 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>
<description>International audience</description>
<source>ISSN: 0041-008X</source>
<source>EISSN: 1096-0333</source>
<source>Toxicology and Applied Pharmacology</source>
<publisher>Elsevier</publisher>
<identifier>inserm-00871698</identifier>
<identifier>http://www.hal.inserm.fr/inserm-00871698</identifier>
<source>http://www.hal.inserm.fr/inserm-00871698</source>
<source>Toxicology and Applied Pharmacology, Elsevier, 2012, 261 (1), pp.74-87. 〈10.1016/j.taap.2012.03.014〉</source>
<identifier>DOI : 10.1016/j.taap.2012.03.014</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.taap.2012.03.014</relation>
<identifier>PUBMED : 22483798</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/22483798</relation>
<language>en</language>
<subject lang=en>Mycotoxins</subject>
<subject lang=en>Enniatins</subject>
<subject lang=en>Cytokines</subject>
<subject lang=en>Inflammasome</subject>
<subject lang=en>Apoptosis</subject>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<subject>[SDV.CAN] Life Sciences [q-bio]/Cancer</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The mycotoxin enniatin B (EnnB) is predominantly produced by species of the Fusarium genera, and often found in grain. The cytotoxic effect of EnnB has been suggested to be related to its ability to form ionophores in cell membranes. The present study examines the effects of EnnB on cell death, differentiation, proliferation and pro-inflammatory responses in the murine monocyte-macrophage cell line RAW 264.7. Exposure to EnnB for 24 h caused an accumulation of cells in the G0/G1-phase with a corresponding decrease in cyclin D1. This cell cycle-arrest was possibly also linked to the reduced cellular ability to capture and internalize receptors as illustrated by the lipid marker ganglioside GM1. EnnB also increased the number of apoptotic, early apoptotic and necrotic cells, as well as cells with elongated spindle-like morphology. The Neutral Red assay indicated that EnnB induced lysosomal damage; supported by transmission electron microscopy (TEM) showing accumulation of lipids inside the lysosomes forming lamellar structures/myelin bodies. Enhanced levels of activated caspase-1 were observed after EnnB exposure and the caspase-1 specific inhibitor ZYVAD-FMK reduced EnnB-induced apoptosis. Moreover, EnnB increased the release of interleukin-1 beta (IL-1β) in cells primed with lipopolysaccharide (LPS), and this response was reduced by both ZYVAD-FMK and the cathepsin B inhibitor CA-074Me. In conclusion, EnnB was found to induce cell cycle arrest, cell death and inflammation. Caspase-1 appeared to be involved in the apoptosis and release of IL-1β and possibly activation of the inflammasome through lysosomal damage and leakage of cathepsin B.</description>
<date>2012-05-15</date>
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