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Neural stem cells and cell death.

S Ceccatelli1, C Tamm, E Sleeper

  • 1Division of Toxicology and Neurotoxicology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, Stockholm S-171 77, Sweden. sandra.ceccatelli@imm.ki.se

Toxicology Letters
|April 20, 2004
PubMed
Summary
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Neural stem cells (NSCs) undergo apoptosis via the mitochondrial pathway, involving cytochrome c release and caspase-3 activation, when exposed to neurotoxic insults. The Fas-dependent cell death pathway is not active in these cells.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Neural stem cells (NSCs) are crucial for neural development and undergo programmed cell death (apoptosis).
  • Understanding the mechanisms of NSC apoptosis is vital for comprehending neural development and disease.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying neural stem cell apoptosis induced by neurotoxic insults.
  • To differentiate between the roles of the mitochondrial and Fas-dependent pathways in NSC cell death.

Main Methods:

  • Primary cultures of adult rat brain subventricular zone NSCs and the C17.2 neural stem cell line were used.
  • Cells were exposed to staurosporine and 2,3-dimethoxy-1,4-naphthoquinone (DMNQ) to induce apoptosis.
  • Apoptosis was assessed via morphology, TUNEL staining, Annexin V labeling, cytochrome c release, caspase-3 activity, and Fas receptor signaling.

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Main Results:

  • NSCs exhibited apoptotic morphology, DNA fragmentation, and phosphatidyl serine exposure upon exposure to staurosporine and DMNQ.
  • Mitochondrial release of cytochrome c and activation of caspase-3 were observed, with apoptosis inhibited by a pan-caspase inhibitor.
  • While NSCs express Fas receptor and procaspase-8, Fas agonistic antibody failed to induce apoptosis, suggesting the Fas pathway is inactive for cell death.

Conclusions:

  • The mitochondrial pathway, involving cytochrome c release and caspase-3 activation, is the primary mechanism for neurotoxic insult-induced apoptosis in these neural stem cells.
  • The Fas-dependent cell death pathway is not operative in these NSC models.
  • Fas signaling in NSCs may instead mediate growth signals via ERK pathway activation.