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Role of oxidative stress and caspase 3 in CD47-mediated neuronal cell death

Changhong Xing1, Sunryung Lee, Woo Jean Kim

  • 1Neuroprotection Research Laboratory, Department of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, MA 02129, USA.

Journal of Neurochemistry
|November 18, 2008
PubMed

Insights

CD47 signaling induces neuronal cell death via parallel pathways involving oxidative stress and caspase activation. These findings reveal CD47

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • CD47 (integrin-associated protein) is known to induce cell death in blood and tumor cells.
  • Recent research indicates CD47 signaling also occurs in neurons.

Purpose of the Study:

  • To investigate the role of CD47 in neuronal cell death.
  • To elucidate the mechanisms by which CD47 influences neuron survival.

Main Methods:

  • Primary mouse cortical neurons were exposed to the CD47 ligand thrombospondin-1 or the activating peptide 4N1K.
  • Levels of active caspase 3 and reactive oxygen species (ROS) were measured.
  • The effects of ROS scavengers and caspase inhibitors on cell death were assessed.

Main Results:

  • CD47 activation by thrombospondin-1 or 4N1K induced neuronal cell death.
  • Active caspase 3 levels and ROS generation increased in a time-dependent manner following CD47 activation.
  • Both ROS scavengers and caspase inhibitors reduced cell death, but ROS scavenging did not affect caspase 3 activation.
  • Combined treatment with caspase inhibitors and ROS scavengers did not provide additive protection.

Conclusions:

  • CD47 mediates neuronal cell death through parallel and redundant pathways involving oxidative stress and caspase activation.
  • These pathways appear to be both caspase-dependent and caspase-independent.

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