Inhibition of IκBα phosphorylation prevents glutamate-induced NF-κB activation and neuronal cell death

M. Pizzi, I. Sarnico, F. Boroni, A. Benetti, M. Benarese, P. F. Spano

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

NF-κB is a nuclear transcription factor involved in the control of fundamental cellular functions including regulation of cell survival. We investigated NF-κB activation induced by two opposing modulators of cell viability: IL-1β and glutamate. We found that IL-1β activated p50, p65 and c-Rel subunits of NF-κB, while glutamate activated only p50 and p65 proteins. Cell stimulation by glutamate, correlated with expression of the pro-apoptotic genes Caspase-3, Caspase-2L and Bax. Conversely, IL-1β induced the expression of the short anti-apoptotic isoform of Caspase-2. Finally, we analysed the effect of the inhibition of IκBα degradation on glutamate-induced toxicity by using BAY 11-7082, a selective inhibitor of IκBα phosphorylation. Our results suggest that BAY 11-7082 preserves neuron viability from the glutamate-mediated injury.

Original languageEnglish
Title of host publicationActa Neurochirurgica, Supplementum
Pages59-63
Number of pages5
Edition93
DOIs
Publication statusPublished - 2005

Publication series

NameActa Neurochirurgica, Supplementum
Number93
ISSN (Print)00651419

Keywords

  • Bay 11-7082
  • Glutamate
  • IL-1β
  • NF-κB, p65

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery
  • Medicine(all)

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    Pizzi, M., Sarnico, I., Boroni, F., Benetti, A., Benarese, M., & Spano, P. F. (2005). Inhibition of IκBα phosphorylation prevents glutamate-induced NF-κB activation and neuronal cell death. In Acta Neurochirurgica, Supplementum (93 ed., pp. 59-63). (Acta Neurochirurgica, Supplementum; No. 93). https://doi.org/10.1007/3-211-27577-0-8