Death effector activation in the subventricular zone subsequent to perinatal hypoxia/ischemia

Michael J. Romanko, Changlian Zhu, Ben A. Bahr, Klas Blomgren, Steven W. Levison

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Perinatal hypoxia/ischemia (H/I) is the leading cause of neurological injury resulting from birth complications and pre-maturity. Our studies have demonstrated that this injury depletes the subventricular zone (SVZ) of progenitors. In this study, we sought to reveal which cell death pathways are activated within these progenitors after H/I. We found that calpain activity is detected as early as 4 h of reperfusion and is sustained for 48 h, while caspase 3 activation does not occur until 8 h and peaks at 24 h post-insult. Activated calpains and caspase 3 co-localized within precursors situated in the lateral aspects of the SVZ (which coincides with progenitor cell death), whereas neither enzyme was activated in the medial SVZ (which harbors the neural stem cells that are resilient to this insult). These studies reveal targets for neuroprotective agents to protect precursors from cell death towards the goal of restoring normal brain development after H/I.

Original languageEnglish (US)
Pages (from-to)1121-1131
Number of pages11
JournalJournal of neurochemistry
Issue number3
StatePublished - Nov 2007

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience


  • Apoptosis
  • Calpains
  • Caspases
  • Development
  • Oligodendrocytes
  • Stem cells
  • Stroke


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