IκB overexpression in cardiomyocytes prevents NF-κB translocation and provides cardioprotection in trauma

Deborah L. Carlson, D. Jean White, David L. Maass, Robin C. Nguyen, Brett Giroir, Jureta W. Horton

Research output: Contribution to journalArticle

32 Scopus citations

Abstract

This study examined the effects of either IκBα overexpression (transgenic mice) or N-acetyl-leucinyl-leucinyl-norleucinal (ALLN) administration (proteosome inhibitor in wild-type mice) on cardiomyocyte secretion of tumor necrosis factor-α (TNF-α) and on cardiac performance after burn trauma. Transgenic mice were divided into four experimental groups. IκBα overexpressing mice were given a third-degree scald burn over 40% of the total body surface area or wild-type littermates were given either a scald or sham burn to provide appropriate controls. Pharmacological studies included ALLN (20 mg/kg) administration in either burned wild-type mice or wild-type shams. Burn trauma in wild-type mice promoted nuclear factor-κB (NF-κB) nuclear translocation, cardiomyocyte secretion of TNF-α, and impaired cardiac performance. IκBα overexpression or ALLN treatment of burn trauma prevented NF-κB activation in cardiac tissue, prevented cardiomyocyte secretion of TNF-α, and ablated burn-mediated cardiac contractile dysfunction. These data suggest that NF-κB activation and inflammatory cytokine secretion play a significant role in post-burn myocardial abnormalities.

Original languageEnglish (US)
Pages (from-to)H804-H814
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume284
Issue number3 53-3
DOIs
StatePublished - Mar 1 2003

Keywords

  • Cardiac contractile function
  • Collagenase digestion
  • Fura 2-AM
  • N-acetyl-leucinyl-leucinyl-norleucinal

ASJC Scopus subject areas

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

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