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Pathophysiological factors affecting CAR gene expression.

Jean Marc Pascussi1, Zdenek Dvorák, Sabine Gerbal-Chaloin

  • 1INSERM 128, Montpellier, France. pascussi@montp.inserm.fr

Drug Metabolism Reviews
|January 7, 2004
PubMed
Summary
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The glucocorticoid receptor (GR) regulates the constitutive androstane receptor (CAR), a key player in drug detoxification. Inhibiting GR function reduces CAR expression and drug-metabolizing enzyme activity, impacting detoxification processes.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Hepatology

Background:

  • The body eliminates harmful compounds via enzymes and transporters.
  • Constitutive androstane receptor (CAR) controls genes for drug metabolism and bilirubin clearance.
  • CAR is activated by xenobiotics and endogenous compounds.

Purpose of the Study:

  • Investigate molecular mechanisms of CAR gene expression in human hepatocytes.
  • Identify CAR as a glucocorticoid receptor (GR) target gene.
  • Test the hypothesis that GR activation is critical for CAR-mediated cellular response.

Main Methods:

  • Studied CAR gene expression in human hepatocytes.
  • Investigated the effect of microtubule disrupting agents (MIAs) and proinflammatory cytokines on GR and CAR.

Related Experiment Videos

  • Analyzed GR inhibition via JNK, AP-1, and NF-kB pathways.

    • Main Results:

    • Identified CAR as a GR target gene.
    • Demonstrated that GR inhibition decreases CAR gene expression.
    • Showed that MIAs and cytokines inhibit phenobarbital-mediated CYP gene expression.

    Conclusions:

    • GR activation plays a critical role in CAR-mediated cellular response.
    • Chemicals or pathophysiological factors affecting GR function decrease CAR function.
    • GR inhibition impacts drug detoxification by reducing CAR and CYP gene expression.