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A disintegrin and metalloprotease 10 (ADAM10) is a central regulator of murine liver tissue homeostasis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F16%3A00473055" target="_blank" >RIV/68378050:_____/16:00473055 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.18632/oncotarget.7836" target="_blank" >http://dx.doi.org/10.18632/oncotarget.7836</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.18632/oncotarget.7836" target="_blank" >10.18632/oncotarget.7836</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    A disintegrin and metalloprotease 10 (ADAM10) is a central regulator of murine liver tissue homeostasis

  • Original language description

    A Disintegrin And Metalloprotease (ADAM) 10 exerts essential roles during organ development and tissue integrity in different organs, mainly through activation of the Notch pathway. However, only little is known about its implication in liver tissue physiology. Here we show that in contrast to its role in other tissues, ADAM10 is dispensable for the Notch2-dependent biliary tree formation. However, we demonstrate that expression of bile acid transporters is dependent on ADAM10. Consequently, mice deficient for Adam10 in hepatocytes, cholangiocytes and liver progenitor cells develop spontaneous hepatocyte necrosis and concomitant liver fibrosis. We furthermore observed a strongly augmented ductular reaction in 15-week old ADAM10(Delta hep/Delta ch) mice and demonstrate that c-Met dependent liver progenitor cell activation is enhanced. Additionally, liver progenitor cells are primed to hepatocyte differentiation in the absence of ADAM10. These findings show that ADAM10 is a novel central node controlling liver tissue homeostasis. Highlights: Loss of ADAM10 in murine liver results in hepatocyte necrosis and concomitant liver fibrosis. ADAM10 directly regulates expression of bile acid transporters but is dispensable for Notch2-dependent formation of the biliary system.Activation of liver progenitor cells is enhanced through increased c-Met signalling, in the absence of ADAM10. Differentiation of liver progenitor cells to hepatocytes is augmented in the absence of ADAM10.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    OncoTarget

  • ISSN

    1949-2553

  • e-ISSN

  • Volume of the periodical

    7

  • Issue of the periodical within the volume

    14

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    11

  • Pages from-to

    17431-17441

  • UT code for WoS article

    000375699000014

  • EID of the result in the Scopus database