Regulation of the S100B gene by α1-adrenergic stimulation in cardiac myocytes

James N. Tsoporis, Alexander Marks, Linda J. Van Eldik, David O'Hanlon, Thomas G. Parker

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


We previously reported that S100B, a 20-kDa Ca2+-binding homodimer, inhibited the postinfarct myocardial hypertrophic response mediated by α1-adrenergic stimulation through the protein kinase C (PKC) signaling pathway. In the present study, we examined whether the same pathway induced the S100B gene, supporting the hypothesis that S100B is a feedback negative regulator of this pathway. We transfected cultured neonatal rat cardiac myocytes with a luciferase reporter gene driven by the maximal human S100B promoter and progressively shorter segments of this promoter sequentially deleted from the 5′ end. We identified a basic promoter essential for transcription spanning 162 bp upstream of the transcription initiation site and positive (at -782/-162 and -6,689/-4,463) and negative (at -4,463/-782) myocyte-selective regulatory elements. We showed that the basic and maximal S100B promoters were activated specifically by α1-adrenergic agonists through the α1A-adrenergic receptor, but not by any other trophic hormonal stimuli. The activation of the S100B promoter was mediated through the PKC signaling pathway. Transcription enhancer factor-1 (TEF-1) and related to TEF-1 (RTEF-1) influenced transcription from the maximal, but not the basic, promoter implicating active MCAT elements upstream from the basic promoter. Acting in opposing fashions, TEF-1 transrepressed the S100B promoter and RTEF-1 transactivated the promoter. Our results suggest that α1-adrenergic stimulation induces the S100B gene after myocardial infarction through the PKC signaling pathway and that this induction is modulated by TEF-1 and RTEF-1.

Original languageEnglish
Pages (from-to)H193-H203
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1 53-1
StatePublished - Jan 1 2003


  • Norepinephrine
  • TEF-1

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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