Journal
CELL DEATH AND DIFFERENTIATION
Volume 10, Issue 3, Pages 365-370Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401158
Keywords
Bax; BH3; cytochrome c; brain mitochondria; nerve growth factor; pheochromocytoma
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Funding
- NINDS NIH HHS [R01NS34152] Funding Source: Medline
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dBax mediates cytochrome c release and apoptosis during neurodevelopment. Brain mitochondria that were isolated from 8-day, 17-day, and adult rats displayed decreasing levels of mitochondrial Bax. The amount of cytochrome c released from brain mitochondria by a peptide containing the BH3 cell death domain decreased with increasing age. However, approximately 60% of cytochrome c in adult brain mitochondria could be released by the BH3 peptide in the presence of exogenous human recombinant Bax. Mitochondrial Bax was downregulated in PC12S neural cells differentiated with nerve growth factor, and mitochondria isolated from these cells demonstrated decreased sensitivity to BH3-peptide-induced cytochrome c release. These results demonstrate that immature brain mitochondria and mitochondria from undifferentiated neural cells are particularly sensitive to cytochrome c release mediated by endogenous Bax and a BH3 death domain peptide. Postnatal developmental changes in mitochondrial Bax levels may contribute to the increased susceptibility of neurons to pathological apoptosis in immature animals.
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