Microglial apoptosis induced by chromogranin A is mediated by mitochondrial depolarisation and the permeability transition but not by cytochrome c release

J Neurochem. 2000 Apr;74(4):1452-62. doi: 10.1046/j.1471-4159.2000.0741452.x.

Abstract

Chromogranin A is up-regulated in the senile plaques of Alzheimer's brain and is a novel activator of microglia, transforming them to a neurotoxic phenotype. Treatment of primary cultures of rat brain microglia or the murine N9 microglial cell line with chromogranin A resulted in nitric oxide production, which triggered microglial apoptosis. Exposure of microglia to chromogranin A resulted in a fall in mitochondrial membrane potential. Mitochondrial depolarisation and apoptosis were reduced significantly by cyclosporin A, but not by the calcineurin inhibitor FK506. Cytochrome c did not translocate from the mitochondria to the cytosol, but its expression became significantly enhanced within the mitochondria. Inhibition of caspase 1 attenuated chromogranin A-induced microglial apoptosis, but did not prevent mitochondrial depolarisation, indicating that apoptosis occurred downstream of mitochondrial depolarisation. Conversely, staurosporine-induced microglial apoptosis led to mitochondrial cytochrome c release, but not caspase 1 activation. Our findings provide insight into the pathways controlling activation-triggered microglial apoptosis and may point to routes for the modulation of microglial evoked neurotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate / metabolism
  • Adenosine Triphosphate / metabolism
  • Animals
  • Apoptosis / drug effects*
  • Biomarkers, Tumor / pharmacology*
  • Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
  • Caspase 1 / metabolism
  • Cell Membrane Permeability / drug effects
  • Cell Membrane Permeability / physiology
  • Cells, Cultured
  • Chromogranin A
  • Chromogranins / pharmacology*
  • Cysteine Proteinase Inhibitors / pharmacology
  • Cytochrome c Group / metabolism*
  • Cytosol / metabolism
  • Enzyme Inhibitors / pharmacology
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Microglia / cytology*
  • Microglia / enzymology
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / metabolism
  • Oligopeptides / pharmacology
  • Rats
  • Staurosporine / pharmacology
  • Uncoupling Agents / pharmacology

Substances

  • Biomarkers, Tumor
  • Chromogranin A
  • Chromogranins
  • Cysteine Proteinase Inhibitors
  • Cytochrome c Group
  • Enzyme Inhibitors
  • Oligopeptides
  • Uncoupling Agents
  • benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone
  • chromogranin A, rat
  • L 709049
  • Nitric Oxide
  • Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
  • Adenosine Diphosphate
  • Adenosine Triphosphate
  • Nitric Oxide Synthase
  • Caspase 1
  • Staurosporine