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Maturation-dependent oligodendrocyte apoptosis caused by hyperoxia

Bettina Gerstner1, Christoph Bührer, Cornelia Rheinländer

  • 1Department of Neonatology, Charité Campus Virchow-Klinikum, Berlin, Germany. bettina.gerstner@childrens.harvard.edu

Journal of Neuroscience Research
|May 5, 2006
PubMed

Insights

High oxygen levels harm immature brain cells, increasing the risk of cerebral palsy. This study shows hyperoxia causes apoptosis in immature oligodendrocytes, a key cell for brain development.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Periventricular leukomalacia (PVL) is a major cause of cerebral palsy in preterm infants.
  • PVL predominantly affects white matter during critical periods of oligodendrocyte development (23-32 weeks postconceptional age).
  • The rise in oxygen levels at birth and during neonatal intensive care may injure immature oligodendrocytes.

Purpose of the Study:

  • To investigate the effects of hyperoxia on oligodendrocytes (OLs) at different maturation stages.
  • To determine if hyperoxia induces cell death in immature and mature OLs.
  • To elucidate the mechanisms underlying hyperoxia-induced OL injury.

Main Methods:

  • In vitro studies using rat oligodendroglia cell lines (immature OLs, pre-OLs, mature OLs) exposed to 80% hyperoxia.
  • In vivo studies involving hyperoxia exposure in 6-day-old rat pups.
  • Assessment of cell death via flow cytometry (annexin-V) and apoptosis markers (activated caspase-3).
  • Cell viability measured by MTT assay.
  • Effect of caspase inhibitor (zVAD-fmk) on hyperoxia-induced cell death.

Main Results:

  • Hyperoxia induced apoptosis in immature and pre-oligodendrocytes after 24-48 hours.
  • Mature oligodendrocytes showed resistance to hyperoxia.
  • Cell death was confirmed by MTT assay and caspase-3 activation.
  • The pan-caspase inhibitor zVAD-fmk blocked hyperoxia-induced cell death.
  • Degeneration of OLs and caspase-3 activation were observed in vivo in rat brains.

Conclusions:

  • Hyperoxia triggers maturation-dependent apoptosis in immature and pre-oligodendrocytes.
  • Caspase activation is involved in hyperoxia-induced oligodendrocyte cell death.
  • These findings suggest a mechanism relevant to white matter injury in preterm infants.

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