STAT-1 and c-Fos interaction in nitric oxide synthase-2 gene activation

Am J Physiol Lung Cell Mol Physiol. 2003 Jul;285(1):L137-48. doi: 10.1152/ajplung.00441.2002.

Abstract

Interferon-gamma (IFN-gamma) is required for induction of the human nitric oxide synthase-2 (NOS2) gene in lung epithelium. Although the human NOS2 promoter region contains many cytokine-responsive elements, the molecular basis of induction is only partially understood. Here, the major cis-regulatory elements that control IFN-gamma-inducible NOS2 gene transcription in human lung epithelial cells are identified as composite response elements that bind signal transducer and activator of transcription 1 (STAT-1) and activator protein 1 (AP-1), which is comprised of c-Fos, Fra-2, c-Jun, and JunD. Notably, IFN-gamma activation of the human NOS2 promoter is shown to require functional AP-1 regulatory region(s), suggesting a role for AP-1 activation/binding in the IFN-gamma induction of genes. We show that c-Fos interacts with STAT-1 after IFN-gamma activation and the c-Fos/STAT-1 complex binds to the gamma-activated site (GAS) element in close proximity to AP-1 sites located at 4.9 kb upstream of the transcription start site. Taken together, our findings support a model in which a physical interaction between c-Fos and STAT-1 participates in NOS2 gene transcriptional activation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 5' Flanking Region / genetics
  • Antineoplastic Agents / pharmacology
  • Base Sequence
  • Cells, Cultured
  • DNA-Binding Proteins / metabolism*
  • Enzyme Induction / drug effects
  • Enzyme Induction / physiology
  • Gene Expression Regulation, Enzymologic / drug effects
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-1 / pharmacology
  • Molecular Sequence Data
  • Mutagenesis / physiology
  • Nitric Oxide Synthase / genetics*
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Oligodeoxyribonucleotides, Antisense / pharmacology
  • Promoter Regions, Genetic / physiology
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / enzymology*
  • STAT1 Transcription Factor
  • Signal Transduction / physiology
  • Trans-Activators / metabolism*
  • Transcription Factor AP-1 / metabolism
  • Transcriptional Activation
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Antineoplastic Agents
  • DNA-Binding Proteins
  • Interleukin-1
  • Oligodeoxyribonucleotides, Antisense
  • Proto-Oncogene Proteins c-fos
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • Trans-Activators
  • Transcription Factor AP-1
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II