Staurosporine-induced apoptosis in P388D1 macrophages involves both extrinsic and intrinsic pathways

Cell Biol Int. 2009 Sep;33(9):1026-31. doi: 10.1016/j.cellbi.2009.06.010. Epub 2009 Jun 12.

Abstract

Treatment of P388D1, a macrophage-like cell line, with staurosporine triggered apoptosis through the activation of caspase-9 and caspase-3. Unexpected effects of staurosporine on the induction of apoptosis were the activation of caspase-8, and an increase of the levels of TNF-alpha. The increased TNF-alpha levels led to activation of caspase-8 by an autocrine effect via the TNF receptor expressed by the P388D1 macrophages. In contrast, P388D1 macrophages that either had been exposed to UV light or treated with dexamethasone did not undergo apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents, Hormonal / pharmacology
  • Apoptosis*
  • Caspase 3 / drug effects
  • Caspase 3 / metabolism
  • Caspase 8 / drug effects
  • Caspase 8 / metabolism
  • Caspase 9 / drug effects
  • Caspase 9 / metabolism
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • DNA Fragmentation / drug effects
  • Dexamethasone / pharmacology
  • Macrophages / drug effects*
  • Macrophages / radiation effects
  • Mice
  • Protein Kinase Inhibitors / pharmacology*
  • Receptors, Tumor Necrosis Factor, Type I / agonists
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Staurosporine / pharmacology*
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / drug effects
  • Ultraviolet Rays / adverse effects

Substances

  • Antineoplastic Agents, Hormonal
  • Protein Kinase Inhibitors
  • Receptors, Tumor Necrosis Factor, Type I
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Caspase 3
  • Caspase 8
  • Caspase 9
  • Staurosporine