BAX Contributes to Apoptotic-Like Death Following Neonatal Hypoxia-Ischemia: Evidence for Distinct Apoptosis Pathways

摘要: Hypoxic-ischemic (H-I) injury to the neonatal brain has been shown result in rapid cell death with features of acute excitotoxicity/necrosis as well prominent delayed apoptosis such marked caspase-3 activation. BAX, a pro-apoptotic molecule, be required for apoptotic neuronal during normal development but contribution endogenous BAX pathways following H-I developing or adult not studied. Bax +/+, +/−, and −/− mice at post-natal day 7 were subjected unilateral carotid ligation followed by exposure 45 minutes 8% oxygen. At different timepoints H-I, tissue was studied conventional histology, immunohistochemistry, immunofluorescence, Western blotting, enzymatic assay determine extent type amount caspase We found that bax had significantly less (38%) hippocampal loss than expressing bax. Some remaining mice, however, still including evidence nuclear shrinkage Though decreased activation compared density cells activated caspase-8 CA3 region hippocampus did differ between +/− mice. These findings demonstrate plays role regulating central nervous system (CNS) model cerebral palsy. In addition, while appears modulate which is linked receptor activation, may contribute apoptotic-like BAX-independent manner.