Declines in Drp1 and parkin expression underlie DNA damage-induced changes in mitochondrial length and neuronal death.

ABSTRACT: Maintaining proper mitochondrial length is essential for normal mitochondrial function in neurons. Mitochondrial fragmentation has been associated with neuronal cell death caused by a variety of experimental toxic stressors. Despite the fact that oxidative stress is a hallmark of neurodegenerative conditions and aging and the resulting activation of p53 is believed to contribute to the neuropathology, little is still known regarding changes in mitochondrial morphology in p53-dependent neuronal death. Therefore, we specifically addressed the relationship between genotoxic stress, p53 activation, and the regulation of mitochondrial morphology in neurons. In cultured postnatal mouse cortical neurons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elongated mitochondria,

SUBMITTER: Wang DB 

PROVIDER: S-EPMC3711762 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature