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<title lang=en>Oncostatin M induces IL-33 expression in liver endothelial cells in mice and expands ST2+CD4+ lymphocytes</title>
<creator>Arshad, Muhammad Imran</creator>
<creator>Guihard, Pierre</creator>
<creator>Danger, Yannic</creator>
<creator>Noël, Gregory</creator>
<creator>Le Seyec, Jacques</creator>
<creator>Boutet, Marie-Astrid</creator>
<creator>Richards, Carl D.</creator>
<creator>L'Helgoualc'H, Annie</creator>
<creator>Genet, Valentine</creator>
<creator>Lucas-Clerc, Catherine</creator>
<creator>Gascan, Hugues</creator>
<creator>Blanchard, Frédéric</creator>
<creator>Piquet-Pellorce, Claire</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>Physiopathologie de la Résorption Osseuse et Thérapie des Tumeurs Osseuses Primitives ; Université de Nantes (UN) - Institut National de la Santé et de la Recherche Médicale (INSERM)</contributor>
<contributor>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>Laboratoire de biochimie générale ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</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>Centre de Recherche en Sciences et Technologies de l'Information et de la Communication - EA 3804 (CRESTIC) ; Université de Reims Champagne-Ardenne (URCA)</contributor>
<description>International audience</description>
<source>ISSN: 0193-1857</source>
<source>EISSN: 1522-1547</source>
<source>AJP - Gastrointestinal and Liver Physiology</source>
<publisher>American Physiological Society</publisher>
<identifier>hal-01220632</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01220632</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01220632</source>
<source>AJP - Gastrointestinal and Liver Physiology, American Physiological Society, 2015, 309 (7), pp.G542--553. 〈10.1152/ajpgi.00398.2014〉</source>
<identifier>DOI : 10.1152/ajpgi.00398.2014</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpgi.00398.2014</relation>
<identifier>PUBMED : 26251474</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/26251474</relation>
<language>en</language>
<subject lang=en>adenovirus</subject>
<subject lang=en>interleukin-33</subject>
<subject lang=en>ST2</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Interleukin (IL)-33 is crucially involved in liver pathology and drives hepatoprotective functions. However, the regulation of IL-33 by cytokines of the IL-6 family, including oncostatin M (OSM) and IL-6, is not well studied. The aim of the present study was to determine whether OSM mediates regulation of IL-33 expression in liver cells. Intramuscular administration in mice of an adenovirus encoding OSM (AdOSM) leads to increase in expression of OSM in muscles, liver, and serum of AdOSM-infected mice compared with control mice. The increase of circulating OSM markedly regulated mRNA of genes associated with blood vessel biology, chemotaxis, cellular death, induction of cell adhesion molecules, and the alarmin cytokine IL-33 in liver. Steady-state IL-33 mRNA was upregulated by OSM at an early phase (8 h) following AdOSM infection. At the protein level, the expression of IL-33 was significantly induced in liver endothelial cells [liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells] with a peak at 8 days post-AdOSM infection in mice. In addition, we found OSM-stimulated human microvascular endothelial HMEC-1 cells and human LSEC/TRP3 cells showed a significant increase in expression of IL-33 mRNA in a dose-dependent manner in cell culture. The OSM-mediated overexpression of IL-33 was associated with the activation/enrichment of CD4(+)ST2(+) cells in liver of AdOSM-infected mice compared with adenovirus encoding green fluorescent protein-treated control mice. In summary, these data suggest that the cytokine OSM regulates the IL-33 expression in liver endothelial cells in vivo and in HMEC-1/TRP3 cells in vitro and may specifically expand the target CD4(+)ST2(+) cells in liver</description>
<date>2015</date>
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