Interferon-gamma enhances the apoptosis of macrophages under trophic stress through activation of p53 and the JAK1 pathway

Arch Pharm Res. 2010 Feb;33(2):285-91. doi: 10.1007/s12272-010-0214-5. Epub 2010 Feb 24.

Abstract

Apoptosis has been implicated as an important mediator of immunosuppression associated with a depleted nutritional state. Since a number of cytokines are likely to influence the rate of apoptosis, we determined the effect of interferon-gamma (IFN-gamma) on apoptosis of macrophages in serum/amino acid deprived cell culture conditions. IFN-gamma further increased the rate of apoptosis compared to trophically stressed macrophages. In addition, we showed that enhancement of apoptosis by IFN-gamma is caused by a decrease in mitochondrial membrane potential due to upregulation of p53 and Bax and down-regulation of Bcl-xL. Moreover, we found that IFN-gamma increases caspase-3 activity that had been induced by serum/amino acid depletion, and that JAK1 signaling is involved in capase-3 activation and in the enhancement of apoptosis by IFN-gamma.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Ascitic Fluid / metabolism
  • Caspase 3 / metabolism
  • DNA Fragmentation / drug effects
  • Down-Regulation
  • Exudates and Transudates / metabolism
  • Interferon-gamma / pharmacology*
  • Janus Kinase 1 / biosynthesis*
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Membrane Potential, Mitochondrial / drug effects
  • Mice
  • Mice, Inbred C57BL
  • Stress, Physiological
  • Tumor Suppressor Protein p53 / biosynthesis*
  • Up-Regulation
  • bcl-2-Associated X Protein / biosynthesis*
  • bcl-2-Associated X Protein / metabolism
  • bcl-X Protein / biosynthesis*

Substances

  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • bcl-X Protein
  • Interferon-gamma
  • Janus Kinase 1
  • Caspase 3