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- J H Sung, H Zhao, M Roy, R M Sapolsky, and G K Steinberg.
- Department of Neurosurgery, Stanford University, School of Medicine, 300 Pasteur Drive R200, Stanford, CA 94305-5327, USA.
- Neuroscience. 2007 Nov 23; 149 (4): 804-12.
AbstractApoptosis, a predominant cause of neuronal death after stroke, can be executed in a caspase-dependent or apoptosis inducing factor (AIF)-dependent manner. Herpes simplex virus (HSV) vectors expressing caspase inhibitors p35 and crmA have been shown to be neuroprotective against various excitotoxic insults. Here we further evaluated the possible neuroprotective role of p35 and crmA in a rat stroke model. Overexpression of p35, but not crmA, significantly increased neuronal survival. Results of double immunofluorescence staining indicate that compared with neurons infected with crmA or control vectors, p35-infected neurons had less active caspase-3 expression, cytosolic cytochrome c and nuclear AIF translocation.
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