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1.  Viral caspase inhibitor p35, but not crmA, is neuroprotective in the ischemic penumbra following experimental stroke 
Neuroscience  2007;149(4):804-812.
Apoptosis, 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.
doi:10.1016/j.neuroscience.2007.07.030
PMCID: PMC2144739  PMID: 17945431
cerebral ischemia; apoptosis; caspase inhibitor; crmA; p35; gene therapy; stroke

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