%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 }