IFN-γ inhibits AP-1 binding activity in human brain-derived cells through a nitric oxide dependent mechanism

Katherine Conant, Umbereen Ahmed, Joan P. Schwartz, Eugene O. Major

Research output: Contribution to journalArticle

Abstract

It has been demonstrated that CNS levels of the cytokine IFN-γ are elevated in association with a number of neuro-inflammatory diseases. In the present study, we have examined the effect of this cytokine on human brain derived cells. We show that prolonged treatment (22 h) of such cells with IFN-γ inhibits the DNA binding activity of transcription factor AP-1. Furthermore, we show that this effect can be reversed by either N(G)- monomethyl-L-arginine (L-NMMA) or L-N5-(1-iminoethyl)ornithine (L-NIO), competitive inhibitors of nitric oxide synthase activity [Rees et al., 1990]. In addition, we show that treatment of brain-derived cells with the nitric oxide donor 3-morpholinosydnonimine, HCl (SIN-1), or [N-(b-D-glucopyranosyl)- N2-acetyl-S-nitroso-D,L-penicillaminamide] (glyco-SNAP-1), also inhibits the binding activity of AP-1. Together, these results suggest that IFN-γ can inhibit AP-1 binding activity through a nitric oxide dependent mechanism.

Original languageEnglish (US)
Pages (from-to)39-44
Number of pages6
JournalJournal of Neuroimmunology
Volume88
Issue number1-2
DOIs
StatePublished - Aug 1 1998

Keywords

  • Astrocytes
  • Interferon-γ
  • Neurons
  • Nitric oxide
  • Nitric oxide synthase
  • Transcription factor AP-1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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