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Regulation of the S100B gene by alpha 1-adrenergic stimulation in cardiac myocytes

James N Tsoporis1, Alexander Marks, Linda J Van Eldik

  • 1Division of Cardiology, Department of Medicine, The Toronto General Hospital Research Institute, University of Toronto, Ontario M5G 1L6, Canada.

American Journal of Physiology. Heart and Circulatory Physiology
|October 22, 2002
PubMed

Insights

Alpha(1)-adrenergic stimulation induces the S100B gene via the protein kinase C (PKC) pathway after myocardial infarction. This process is modulated by transcription factors TEF-1 and RTEF-1, suggesting S100B acts as a negative feedback regulator.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Gene Regulation

Background:

  • S100B, a calcium-binding protein, was previously found to inhibit post-infarct myocardial hypertrophy mediated by alpha(1)-adrenergic stimulation via protein kinase C (PKC).
  • This study investigates if the same pathway also induces the S100B gene, proposing S100B as a negative feedback regulator.

Purpose of the Study:

  • To determine if alpha(1)-adrenergic stimulation induces the S100B gene through the PKC signaling pathway.
  • To identify regulatory elements within the S100B promoter responsive to this stimulation.
  • To elucidate the roles of transcription factors TEF-1 and RTEF-1 in S100B gene regulation.

Main Methods:

  • Transfection of cultured neonatal rat cardiac myocytes with luciferase reporter constructs driven by the S100B promoter and its deletion mutants.
  • Treatment with alpha(1)-adrenergic agonists and other hormonal stimuli.
  • Analysis of promoter activity and the influence of transcription factors TEF-1 and RTEF-1.

Main Results:

  • A basic promoter essential for S100B transcription was identified (-162 bp).
  • Positive and negative myocyte-selective regulatory elements were mapped within the promoter.
  • Alpha(1)-adrenergic agonists, via the alpha(1A)-receptor and PKC pathway, specifically activated the S100B promoter.
  • TEF-1 repressed and RTEF-1 activated S100B transcription, particularly from the maximal promoter, indicating MCAT element involvement.

Conclusions:

  • Alpha(1)-adrenergic stimulation induces S100B gene expression post-myocardial infarction through the PKC pathway.
  • S100B gene induction is modulated by the opposing actions of TEF-1 and RTEF-1.
  • These findings support the hypothesis that S100B functions as a negative feedback regulator in this pathway.

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