Induction of ref-1 ensures AP-1 activation in intracellular oxidative environment of IL-2-stimulated BA/F3beta cells

Biochem Biophys Res Commun. 2000 Nov 19;278(2):462-9. doi: 10.1006/bbrc.2000.3826.

Abstract

Our previous study of interleukin-2 (IL-2) signaling found that redox factor-1 (Ref-1) mRNA was upregulated by IL-2. In this study, we further studied the function of Ref-1 in the potential redox regulation of IL-2 signaling in BA/F3beta cells. Western blot analysis confirmed that IL-2 stimulation increases Ref-1 protein. Flow cytometric assay by using 2',7'-dichlorofluorescin diacetate indicated that IL-2 stimulation results in an oxidative shift of intracellular environment. However, IL-2-induced activator protein-1 (AP-1) is oxidation-sensitive. Gel shift assays of nuclear extracts immunodepleted of Ref-1 protein demonstrated that IL-2-induced AP-1 DNA binding is dependent on the presence of Ref-1. This was further confirmed by the restoration of AP-1 DNA binding upon the re-addition of immunoprecipitated Ref-1. Additionally, reporter gene assays showed that AP-1 transcriptional activity was enhanced by the overexpression of Ref-1 and attenuated by the introduction of antisense Ref-1. These results suggest that the induction of Ref-1 ensures AP-1 activation in the intracellular oxidative environment of IL-2-stimulated BA/F3beta cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Carbon-Oxygen Lyases / biosynthesis*
  • Cell Line
  • DNA Primers
  • DNA-(Apurinic or Apyrimidinic Site) Lyase*
  • Interleukin-2 / pharmacology*
  • Oxidative Stress*
  • Protein Binding
  • Transcription Factor AP-1 / metabolism*

Substances

  • DNA Primers
  • Interleukin-2
  • Transcription Factor AP-1
  • Carbon-Oxygen Lyases
  • DNA-(Apurinic or Apyrimidinic Site) Lyase