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Related Experiment Videos

Cytokines increase CRE binding but decrease CRE-mediated reporter activity in rat hepatocytes by increasing c-Jun.

Baochun Zhang1, Shubing Liu, Michele D Perpetua

  • 1Department of Surgery, University of Pittsburgh, Pittsburgh, PA, USA.

Hepatology (Baltimore, Md.)
|May 4, 2004
PubMed
Summary
This summary is machine-generated.

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Inflammation alters cyclic AMP response element (CRE) binding in liver cells, impacting gene expression during sepsis. This study reveals how cytokines and lipopolysaccharide affect CRE activity and transcription in hepatocytes.

Area of Science:

  • Hepatocyte biology
  • Molecular mechanisms of inflammation
  • Gene regulation

Background:

  • The cyclic AMP response element (CRE) regulates genes vital for hepatocyte function.
  • CRE sites are present in genes involved in inflammation, but their role in hepatocytes during inflammation is unclear.

Purpose of the Study:

  • To investigate the regulation of CRE-mediated transcription in hepatocytes during inflammatory conditions like sepsis.

Main Methods:

  • Hepatocytes were stimulated with proinflammatory cytokines in vitro and rats were injected with lipopolysaccharide (LPS) in vivo.
  • Electromobility shift assay (EMSA) measured CRE binding activity.
  • CRE-dependent reporter gene activity was assessed, and JNK inhibition was employed.

Main Results:

Related Experiment Videos

  • Cytokines and LPS increased CRE binding activity in hepatocytes.
  • However, CRE-dependent reporter activity decreased with cytokine stimulation.
  • JNK inhibition reversed increased CRE binding and restored reporter activity.
  • Supershift assays identified CREB and c-Jun within the CRE binding complex, with CREB inducing and c-Jun suppressing reporter activity.

Conclusions:

  • Proinflammatory cytokines modulate CRE binding and activity in cultured hepatocytes.
  • Sepsis-induced alterations in CRE binding likely contribute to the cellular inflammatory response.