Zinc attenuates tnf-mediated activation of NF-KB in endothelial cells

Patrice Cornell, Shirish Barve, Swati Joshibarve, Craig J. McClain, Bernhard Hennig

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Endothelial cell dysfunction which contributes to atherosclerosis may be associated with activation of oxidative stress sensitive transcription factors such as nuclear factor kappa B (NF-KB), enhanced cytokine production and activity and alterations in adhesive properties of the endothelial surface. Zinc, a critical element in the maintenance of normal endothelial integrity, may protect against oxidative stress mediated by inflammatory cytokines. To investigate this hypothesis, endothelial cells were exposed to zinc-deficient media with or without zinc supplementation and then challenged with TNF. Subsequently, nuclear extracts were analyzed for NF-KB binding. Zinc supplementation resulted in a 90% increase in cellular zinc content. Cells cultured in zinc-deficient media expressed significant NF-KB binding which was not demonstrated in zincsupplemented cultures. It was also shown that a 1.5 h exposure to TNF (100 U/mL medium) significantly upregulated NF-KB expression, which was prevented by prior supplementation with physiological levels of zinc. These data suggest that zinc may block the inflammatory cytokine-mediated activation of oxidative stress sensitive transcription factors. Thus, zinc may have antiatherogenic properties by protecting the integrity of the vascular endothelium against oxidative stress and inflammatory insult.

Original languageEnglish
Pages (from-to)A623
JournalFASEB Journal
Issue number3
StatePublished - 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


Dive into the research topics of 'Zinc attenuates tnf-mediated activation of NF-KB in endothelial cells'. Together they form a unique fingerprint.

Cite this