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<title lang=en>The complexity of ERK1 and ERK2 MAPKs in multiple hepatocyte fate responses.</title>
<creator>Frémin, Christophe</creator>
<creator>Ezan, Frédéric</creator>
<creator>Guegan, Jean-Philippe</creator>
<creator>Gailhouste, Luc</creator>
<creator>Trotard, Maud</creator>
<creator>Le Seyec, Jacques</creator>
<creator>Rageul, Julie</creator>
<creator>Théret, Nathalie</creator>
<creator>Langouët, Sophie</creator>
<creator>Baffet, Georges</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>Université européenne de Bretagne (UEB)</contributor>
<contributor>Institut National de la Santé et de la Recherche Médicale (INSERM U522 and U620); Région Bretagne; Association pour la Recherche contre le Cancer (ARC)</contributor>
<description>International audience</description>
<source>ISSN: 0021-9541</source>
<source>EISSN: 1097-4652</source>
<source>Journal of Cellular Physiology</source>
<publisher>Wiley</publisher>
<identifier>hal-00681056</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-00681056</identifier>
<source>https://hal.archives-ouvertes.fr/hal-00681056</source>
<source>Journal of Cellular Physiology, Wiley, 2012, 227 (1), pp.59-69. 〈10.1002/jcp.22742〉</source>
<identifier>DOI : 10.1002/jcp.22742</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/jcp.22742</relation>
<identifier>PUBMED : 21437905</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/21437905</relation>
<language>en</language>
<subject>[SDV.BC] Life Sciences [q-bio]/Cellular Biology</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Recent reports suggest that extracellular signal-regulated kinase (ERK1) and ERK2 mitogen-activated protein kinases (MAPK) may direct specific biological functions under certain contexts. In this study, we investigated the role of early and sustained epidermal growth factor (EGF) stimulation on long-term hepatocyte differentiation and the possible role of ERK1 and ERK2 in this process. We demonstrate a long-term survival and an elevated level of differentiation up to 3 weeks. The differentiation state of hepatocytes is supported by sustained expression of aldolase B, albumin, and the detoxifying enzymes CYP1A2, 2B2, and 3A23. Similarly to freshly isolated cells, cultured hepatocytes also retain the ability to respond to 3-methylcholanthrene (3MC) and phenobarbital (PB), two known CYP inducers. In addition, we show evidence that continuous MAPK/ERK kinase (MEK) inhibition enhances the level of differentiation. Using RNA interference approaches against ERK1 and ERK2, we demonstrate that this effect requires both ERK1 and ERK2 activity, whereas the specific ERK1 knockdown promotes cell survival and the specific ERK2 knockdown regulates cell proliferation. In conclusion, we demonstrate that early and sustained EGF stimulation greatly extends long-term hepatocyte survival and differentiation, and that inhibition of the ERK1/2 MAPK pathway potentiates these pro-survival/pro-differentiation phenotypes. We clearly attest that specific ERK1 and ERK2 MAPKs determine hepatocyte survival and proliferation, respectively, whereas dual inhibition is required to stabilize a highly differentiated state.</description>
<date>2012-01</date>
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