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Environmental Ligands of the Aryl Hydrocarbon Receptor and Their Effects in Models of Adult Liver Progenitor Cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F16%3A00471988" target="_blank" >RIV/68081707:_____/16:00471988 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1155/2016/4326194" target="_blank" >http://dx.doi.org/10.1155/2016/4326194</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1155/2016/4326194" target="_blank" >10.1155/2016/4326194</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Environmental Ligands of the Aryl Hydrocarbon Receptor and Their Effects in Models of Adult Liver Progenitor Cells

  • Original language description

    The toxicity of environmental and dietary ligands of the aryl hydrocarbon receptor (AhR) in mature liver parenchymal cells is well appreciated, while considerably less attention has been paid to their impact on cell populations exhibiting phenotypic features of liver progenitor cells. Here, we discuss the results suggesting that the consequences of the AhR activation in the cellular models derived from bipotent liver progenitors could markedly differ from those in hepatocytes. In contact-inhibited liver progenitor cells, the AhR agonists induce a range of effects potentially linked with tumor promotion. They can stimulate cell cycle progression/proliferation and deregulate cell-to-cell communication, which is associated with downregulation of proteins forming gap junctions, adherens junctions, and desmosomes (such as connexin 43, E-cadherin, beta-catenin, and plakoglobin), as well as with reduced cell adhesion and inhibition of intercellular communication. At the same time, toxic AhR ligands may affect the activity of the signaling pathways contributing to regulation of liver progenitor cell activation and/or differentiation, such as downregulation of Wnt/beta-catenin and TGF-beta signaling, or upregulation of transcriptional targets of YAP/TAZ, the effectors of Hippo signaling pathway. These data illustrate the need to better understand the potential role of liver progenitors in the AhR-mediated liver carcinogenesis and tumor promotion.

  • Czech name

  • Czech description

Classification

  • Type

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

  • CEP classification

    BO - Biophysics

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/GA13-07711S" target="_blank" >GA13-07711S: The role of Hippo signaling pathway and organic toxicants in alterations of liver cell function and xenobiotic metabolism</a><br>

  • 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

    STEM CELLS INTERNATIONAL

  • ISSN

    1687-9678

  • e-ISSN

  • Volume of the periodical

    2016

  • Issue of the periodical within the volume

    Č.2016

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    15

  • Pages from-to

  • UT code for WoS article

    000376020000001

  • EID of the result in the Scopus database