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.
%0 Journal Article
%1 Ness2001
%A Ness, J. K.
%A Romanko, M. J.
%A Rothstein, R. P.
%A Wood, T. L.
%A Levison, S. W.
%D 2001
%J Dev Neurosci
%K Animals; Apoptosis; Caspase 3; Caspases; Cerebral Palsy; Ventricles; Female; Hypoxia-Ischemia, Brain; Microscopy, Electron; Neurotoxins; Oligodendroglia; Pregnancy; Rats; Rats, Wistar; Stem Cells
%N 3
%P 203--208
%T Perinatal hypoxia-ischemia induces apoptotic and excitotoxic death of periventricular white matter oligodendrocyte progenitors.
%V 23
%X 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.
@article{Ness2001,
abstract = {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.},
added-at = {2014-07-19T20:54:19.000+0200},
author = {Ness, J. K. and Romanko, M. J. and Rothstein, R. P. and Wood, T. L. and Levison, S. W.},
biburl = {https://www.bibsonomy.org/bibtex/2a6b6179df8f800977f61d793ea24a358/ar0berts},
groups = {public},
interhash = {597dae7a2ed7d2565a29be3be0ee2b05},
intrahash = {a6b6179df8f800977f61d793ea24a358},
journal = {Dev Neurosci},
keywords = {Animals; Apoptosis; Caspase 3; Caspases; Cerebral Palsy; Ventricles; Female; Hypoxia-Ischemia, Brain; Microscopy, Electron; Neurotoxins; Oligodendroglia; Pregnancy; Rats; Rats, Wistar; Stem Cells},
number = 3,
pages = {203--208},
pii = {dne23203},
pmid = {11598321},
timestamp = {2014-07-19T20:54:19.000+0200},
title = {Perinatal hypoxia-ischemia induces apoptotic and excitotoxic death of periventricular white matter oligodendrocyte progenitors.},
username = {ar0berts},
volume = 23,
year = 2001
}