期刊
DEVELOPMENTAL NEUROSCIENCE
卷 23, 期 3, 页码 203-208出版社
KARGER
DOI: 10.1159/000046144
关键词
apoptosis; caspases; cell death; cerebral palsy; neuroglia; oligodendrocytes; rats; stroke
资金
- NICHD NIH HHS [HD 30705] Funding Source: Medline
- NIMH NIH HHS [MH 59950, R01 MH059950] Funding Source: Medline
- NINDS NIH HHS [NS 37560] Funding Source: Medline
Hypoxia-ischemia (HI) is a leading cause of white matter damage, a major contributor to cerebral palsy in premature infants. Preferential white matter damage is believed to result from vulnerability of the immature oligodendrocyte (the pro-OL) to factors elevated during ischemic damage, such as oxygen free radicals and glutamate. In order to determine whether pro-OLs undergo apoptotic death after HI, we analyzed periventricular white matter OLs in P7 rats 4, 12 and 24 h after HI to analyze the time course and mode of cell death. DNA fragmentation was seen at 12 and 24 h of recovery after HI, representing a 17-fold increase over control. In addition, caspase-3 activation was found in NG2+ pro-OLs at 12 h. Electron-microscopic analysis of cell death in the white matter revealed a transition from early necrotic deaths to hybrid cell deaths to classical apoptosis between 4 and 24 h of recovery from HI. The delayed time course of apoptosis in pro-OLs supports the feasibility of interventions to improve clinical outcomes for newborns surviving birth asphyxia. Copyright (C) 2001 S. Karger AG, Basel.
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