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P53-induces neuronal cell death through parallel pathways


, : P53-induces neuronal cell death through parallel pathways. Society for Neuroscience Abstracts 27(1): 301

P53 has been identified as a key regulator of neuronal cell death both after acute injury and during development. The molecular mechanisms by which p53 induces apoptosis in neurons, however, remain unclear. In the present study we investigated the role of Apaf-1 in p53-mediated neuronal cell death. We show that in comparison with wild-type neurons p53-induced cell death in Apaf-1 deficient neurons is significantly delayed and occurs independently of caspase activation. In contrast to wild-type cells, Apaf1-deficient neurons exhibit only partial chromatin condensation and do not label in Tunel assay. Immunofluorescence staining revealed mitochondrial depolarization, and release of cytochrome-c and apoptosis-inducing-factor (AIF) in both wild-type and Apaf1-deficient neurons undergoing cell death. Furthermore, we show that adenoviral-mediated expression of active AIF directly induced cell death in wild-type and Apaf1-deficient neurons. Finally we demonstrate that overexpression of Bcl-2 prevented the p53-mediated release of both cytochrome-c and AIF and protected against p53-induced neuronal cell death. These results indicate that p53-induces neuronal cell death via parallel pathways: (1) an Apaf1-dependent pathway resulting in caspase activation and (2) an Apaf1-independent pathway involving mitochondrial release of AIF.

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