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Differential release of cytochrome c and adenylate kinase in response to various apoptotic triggers



Differential release of cytochrome c and adenylate kinase in response to various apoptotic triggers



Society for Neuroscience Abstracts 26(1-2): Abstract No -579 10



Activation of caspases by cytochrome c after its release from the mitochondria is a point of no return on the path to apoptosis. The mechanism of this release remains a subject of debate. It is possible that cytochrome c release is a consequence of either the opening of a specific channel or a relatively nonspecific rupturing of the outer mitochondrial membrane due to swelling associated with the mitochondrial permeability transition pore. To address this, we have engineered SH-SY5Y cells that stably overexpress the intermembrane space protein adenylate kinase tagged with a carboxy-terminal hemagglutinin epitope (AK-HA). Because it is considerably larger than cytochrome c, AK-HA was used as a marker of nonspecific rupturing or the opening of a large relatively nonspecific channel. After treatment with various apoptogens, subcellular localization of cytochrome c and AK-HA were assessed by western blotting. We have found differential release of cytochrome c and AK-HA in these cells. In response to the apoptotic trigger etoposide, both cytochrome c and AK-HA were released from the mitochondria; whereas, treatment with staurosporine and Actinomycin D resulted solely in release of cytochrome c. We have observed that only a small fraction of the cytochrome c translocated from the mitochondria to the cytoplasm. The amount of cytochrome c released was sufficient to stimulate caspase activation but did not result in respiratory inhibition. Experiments to assess cytochrome c and AK-HA release in response to other apoptotic triggers are ongoing. Thus far, our data suggest that there may be multiple mechanisms for cytochrome c release from the mitochondria. Sponsored in part by NIH NS34154 to ANM.

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