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<datestamp>2017-12-21</datestamp>
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<title lang=en>RIPK1 protects hepatocytes from death in Fas-induced hepatitis</title>
<creator>Filliol, Aveline</creator>
<creator>Farooq, Muhammad</creator>
<creator>Piquet-Pellorce, Claire</creator>
<creator>Genet, Valentine</creator>
<creator>Dimanche-Boitrel, Marie-Thérèse</creator>
<creator>Vandenabeele, Peter</creator>
<creator>Bertrand, Mathieu J. M.</creator>
<creator>Samson, Michel</creator>
<creator>Le Seyec, Jacques</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>Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>This work was supported by the INSERM, The “Ministère de l’Education Nationale de la Recherche et de la Technologie”, the University of Rennes 1, the “Région Bretagne” and the “Ligue contre le cancer, comités du grand Ouest”. Research in the Vandenabeele group is supported by Belgian grants (Interuniversity Attraction Poles, IAP 7/32), Flemish grants (Research Foundation Flanders: FWO G.0875.11, FWO G.0973.11, FWO G.0A45.12 N, FWO G.0172.12, FWO G.0787.13 N, FWO G.0607.13 N, FWO KAN 31528711, FWO KAN 1504813 N, FWO G0E04.16 N), Methusalem grant (BOF16/MET_V/007), Ghent University grants (MRP, GROUP-ID consortium, BOFGOA2014000702), grants from the Foundation against Cancer (F94), and grants from VIB.</contributor>
<description>International audience</description>
<source>ISSN: 2045-2322</source>
<source>EISSN: 2045-2322</source>
<source>Scientific Reports</source>
<publisher>Nature Publishing Group</publisher>
<identifier>hal-01579612</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01579612</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01579612</source>
<source>Scientific Reports, Nature Publishing Group, 2017, 7, pp.9205. 〈10.1038/s41598-017-09789-8〉</source>
<identifier>DOI : 10.1038/s41598-017-09789-8</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-017-09789-8</relation>
<identifier>PUBMED : 28835677</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/28835677</relation>
<language>en</language>
<subject>[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologie</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Hepatocyte death is a central event during liver disease progression, in which immune cells play key roles by activating members of the Tumor Necrosis Factor Receptor Superfamily (TNFRSF), including TNFR1 (TNFRSF1A), Fas (TNFRSF6) and TRAIL-R2 (TNFRSF10B). Receptor Interacting Protein Kinase 1 (RIPK1) emerged as a signaling node downstream of these receptors. In the case of TNFR1, RIPK1 has been demonstrated to paradoxically serve as a scaffold to promote the survival of hepatocytes and as a kinase to kill them. To evaluate whether RIPK1 also protects hepatocytes from death in response to FasL or TRAIL, we took advantage of liver parenchymal cell-specific Ripk1 knockout mice (Ripk1 (LPC-KO)). We found that Ripk1 (LPC-KO) mice, as well as primary hepatocytes derived from them, were more susceptible to Fas-mediated apoptosis than their respective WT counterparts. Fas-induced hepatocyte death was independent of TNF-α signaling. Interestingly, while TRAIL administration did not induce hepatitis in Ripk1 (LPC-KO) mice or in their WT counterparts, its combination with IFN-γ only induced TNF-α dependent apoptosis in the Ripk1 (LPC-KO) mice. Together, our data demonstrate the protective role of RIPK1 downstream of Fas and highlight the general protective function of RIPK1 in hepatocytes exposed to inflammatory conditions, where TNF-α, FasL and/or TRAIL are present.</description>
<date>2017</date>
</dc>
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