untitled
<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd>
<responseDate>2018-01-17T12:08:52Z</responseDate>
<request identifier=oai:HAL:hal-01532060v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request>
<GetRecord>
<record>
<header>
<identifier>oai:HAL:hal-01532060v1</identifier>
<datestamp>2018-01-11</datestamp>
<setSpec>type:ART</setSpec>
<setSpec>subject:sdv</setSpec>
<setSpec>collection:UNIV-RENNES1</setSpec>
<setSpec>collection:IGDR</setSpec>
<setSpec>collection:CNRS</setSpec>
<setSpec>collection:UNIV-AG</setSpec>
<setSpec>collection:UNIV-ANGERS</setSpec>
<setSpec>collection:IRSET</setSpec>
<setSpec>collection:HL</setSpec>
<setSpec>collection:IGDR-SIM</setSpec>
<setSpec>collection:IRSET-HIAEC</setSpec>
<setSpec>collection:IFR140</setSpec>
<setSpec>collection:BIOSIT</setSpec>
<setSpec>collection:UR1-HAL</setSpec>
<setSpec>collection:UR1-SDV</setSpec>
<setSpec>collection:IRSET-2</setSpec>
<setSpec>collection:STATS-UR1</setSpec>
<setSpec>collection:EHESP</setSpec>
<setSpec>collection:UR1-UFR-SVE</setSpec>
<setSpec>collection:IRSET-EHESP</setSpec>
<setSpec>collection:USPC</setSpec>
</header>
<metadata><dc>
<publisher>HAL CCSD</publisher>
<title lang=en>RIPK1 protects hepatocytes from Kupffer cells-mediated TNF-induced apoptosis in mouse models of PAMP-induced hepatitis</title>
<creator>Filliol, Aveline</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>Raguénès-Nicol, Céline</creator>
<creator>Dion, Sarah</creator>
<creator>Farooq, Muhammad</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Vandenabeele, Peter</creator>
<creator>Bertrand, Mathieu J. M.</creator>
<creator>Le Seyec, Jacques</creator>
<creator>Samson, Michel</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>Institut de Génétique et Développement de Rennes (IGDR) ; Université de Rennes 1 (UR1) - Centre National de la Recherche Scientifique (CNRS) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>INSERM</contributor>
<contributor> Ministere de l'Education Nationale de la Recherche et de la Technologie</contributor>
<contributor> University of Rennes 1</contributor>
<contributor> Region Bretagne</contributor>
<contributor> Ligue contre le cancer, comites du grand Ouest</contributor>
<description>International audience</description>
<source>ISSN: 0168-8278</source>
<source>EISSN: 0168-8278</source>
<source>Journal of Hepatology</source>
<publisher>Elsevier</publisher>
<identifier>hal-01532060</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01532060</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01532060</source>
<source>Journal of Hepatology, Elsevier, 2017, 66 (6), pp.1205--1213. 〈10.1016/j.jhep.2017.01.005〉</source>
<identifier>DOI : 10.1016/j.jhep.2017.01.005</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.jhep.2017.01.005</relation>
<identifier>PUBMED : 28088582</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28088582</relation>
<language>en</language>
<subject lang=en>cytokine</subject>
<subject lang=en> acute hepatitis</subject>
<subject lang=en> rip kinase</subject>
<subject lang=en> ripk1</subject>
<subject lang=en> tnf-alpha</subject>
<subject lang=en> lps</subject>
<subject lang=en> cpg-dna</subject>
<subject lang=en> pamps</subject>
<subject lang=en> damps</subject>
<subject lang=en> liver</subject>
<subject lang=en> inflammation</subject>
<subject lang=en> cell death</subject>
<subject>[SDV.GEN] Life Sciences [q-bio]/Genetics</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Background & Aims: The severity of liver diseases is exacerbated by the death of hepatocytes, which can be induced by the sensing of pathogen associated molecular patterns (PAMPs) derived from the gut microbiota. The molecular mechanisms regulating these cell death pathways are poorly documented. In this study, we investigated the role of the receptor interacting protein kinase 1 (RIPK1), a protein known to regulate cell fate decisions, in the death of hepatocytes using two in vivo models of PAMP-induced hepatitis. Methods: Hepatitis was induced in mice by independent injections of two different bacterial PAMPs: lipopolysaccharide (LPS) and unmethylated CpG oligodeoxynucleotide (CpG-DNA) motifs. The role of RIPK1 was evaluated by using mice specifically lacking RIPK1 in liver parenchymal cells (Ripk1(LPC-KO)). Administration of liposome-encapsulated clodronate served to investigate the role of Kupffer cells in the establishment of the disease. Etanercept, a tumor necrosis factor (TNF)-decoy receptor, was used to study the contribution of TNF-alpha during LPS-mediated liver injury. Results: Whereas RIPK1 deficiency in liver parenchymal cells did not trigger basal hepatolysis, it greatly sensitized hepatocytes to apoptosis and liver damage following a single injection of LPS or CpG-DNA. Importantly, hepatocyte death was prevented by previous macrophage depletion or by TNF inhibition. Conclusions: Our data highlight the pivotal function of RIPK1 in maintaining liver homeostasis in conditions of macrophage-induced TNF burst in response to PAMPs sensing. Lay summary: Excessive death of hepatocytes is a characteristic of liver injury. A new programmed cell death pathway has been described involving upstream death ligands such as TNF and downstream kinases such as RIPK1. Here, we show that in the presence of LPS liver induced hepatic injury was due to secretion of TNF by liver macrophages, and that RIPK1 acts as a powerful protector of hepatocyte death. This newly identified pathway in the liver may be helpful in the management of patients to predict their risk of developing acute liver failure. (C) 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.</description>
<date>2017</date>
</dc>
</metadata>
</record>
</GetRecord>
</OAI-PMH>
