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Death effector activation in the subventricular zone subsequent to perinatal hypoxia/ischemia
Author(s) -
Romanko Michael J.,
Zhu Changlian,
Bahr Ben A.,
Blomgren Klas,
Levison Steven W.
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04820.x
Subject(s) - subventricular zone , neuroprotection , calpain , progenitor cell , hypoxia (environmental) , neural stem cell , neurogenesis , programmed cell death , microbiology and biotechnology , ischemia , neuroscience , caspase , biology , apoptosis , medicine , chemistry , stem cell , biochemistry , enzyme , organic chemistry , oxygen
Abstract 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.