Posttranscriptional Regulation of Neuronal Nitric Oxide Synthase Expression by IFN-γ

Research output: Contribution to journalArticle

Abstract

In this report, the mechanism through which interferon-γ (IFN-γ) regulates the expression of nitric oxide synthase (NOS-1) in neurons was examined. We have shown previously that IFN-γ treatment of cells results in a two log inhibition of vesicular stomatitis virus (VSV) production. This inhibition of VSV replication is dependent both in vitro and in vivo on nitric oxide (NO) production by NOS-1. Furthermore, this effect is associated with the increased expression and activity of NOS-1 following IFN-γ treatment. In vitro, exposure to IFN-γ prior to infection with VSV is a prerequisite to establish an effective antiviral state, indicating the necessity for a priming event. Neuroblastoma cells (NB41A3) were treated with IFN-γ or medium and examined for changes in NOS-1 protein and mRNA expression. NOS-1 protein expression was found to be increased after IFN-γ treatment, and this was associated with increases in both neosynthesis and NOS-1 protein stability. NOS-1 transcription and mRNA levels were unaffected by IFN-γ treatment. These data demonstrate that IFN-γ regulates NOS-1 expression through posttranscriptional and posttranslational mechanisms.

Original languageEnglish (US)
Pages (from-to)141-149
Number of pages9
JournalJournal of Interferon and Cytokine Research
Volume24
Issue number2
DOIs
StatePublished - Feb 2004

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Nitric Oxide Synthase Type I
Interferons
Vesicular Stomatitis
Viruses
Messenger RNA
Protein Stability
Virus Replication
Neuroblastoma
Nitric Oxide Synthase
Antiviral Agents
Nitric Oxide
Proteins
Neurons
Infection

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Cell Biology

Cite this

Posttranscriptional Regulation of Neuronal Nitric Oxide Synthase Expression by IFN-γ. / Chesler, David A.; McCutcheon, Jane A.; Reiss, Carol Shoshkes.

In: Journal of Interferon and Cytokine Research, Vol. 24, No. 2, 02.2004, p. 141-149.

Research output: Contribution to journalArticle

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