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Hepatocyte apoptosis is tumor promoting in murine nonalcoholic steatohepatitis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62156489%3A43210%2F20%3A43917516" target="_blank" >RIV/62156489:43210/20:43917516 - isvavai.cz</a>

  • Alternative codes found

    RIV/00179906:_____/20:10408391

  • Result on the web

    <a href="https://doi.org/10.1038/s41419-020-2283-9" target="_blank" >https://doi.org/10.1038/s41419-020-2283-9</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s41419-020-2283-9" target="_blank" >10.1038/s41419-020-2283-9</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Hepatocyte apoptosis is tumor promoting in murine nonalcoholic steatohepatitis

  • Original language description

    Nonalcoholic fatty liver disease is the most common chronic liver disease and may progress to nonalcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). The molecular determinants of this pathogenic progression, however, remain largely undefined. Since liver tumorigenesis is driven by apoptosis, we examined the effect of overt hepatocyte apoptosis in a mouse model of NASH using mice lacking myeloid cell leukemia 1 (Mcl1), a pro-survival member of the BCL-2 protein family. Hepatocyte-specific Mcl1 knockout (Mcl1(hep)) mice and control littermates were fed chow or FFC (high saturated fat, fructose, and cholesterol) diet, which induces NASH, for 4 and 10 months. Thereafter, liver injury, inflammation, fibrosis, and tumor development were evaluated biochemically and histologically. Mcl1(hep) mice fed with the FFC diet for 4 months displayed a marked increase in liver injury, hepatocyte apoptosis, hepatocyte proliferation, macrophage-associated liver inflammation, and pericellular fibrosis in contrast to chow-fed Mcl1(hep) and FFC diet-fed Mcl1-expressing littermates. After 10 months of feeding, 78% of FFC diet-fed Mcl1(hep) mice developed liver tumors compared to 38% of chow-fed mice of the same genotype. Tumors in FFC diet-fed Mcl1(hep) mice were characterized by cytologic atypia, altered liver architecture, immunopositivity for glutamine synthetase, and histologically qualified as HCC. In conclusion, this study provides evidence that excessive hepatocyte apoptosis exacerbates the NASH phenotype with enhancement of tumorigenesis in mice.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10601 - Cell biology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Cell Death &amp; Disease

  • ISSN

    2041-4889

  • e-ISSN

  • Volume of the periodical

    11

  • Issue of the periodical within the volume

    2

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    12

  • Pages from-to

    80

  • UT code for WoS article

    000511398100002

  • EID of the result in the Scopus database

    2-s2.0-85078871083