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Viral caspase inhibitor p35, but not crmA, is neuroprotective in the ischemic penumbra following experimental stroke NEUROSCIENCE Sung, J. H., Zhao, H., Roy, M., Sapolsky, R. M., Steinberg, G. K. 2007; 149 (4): 804-812

Abstract

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.

View details for DOI 10.1016/j.neuroscience.2007.07.030

View details for Web of Science ID 000251501700008

View details for PubMedID 17945431

View details for PubMedCentralID PMC2144739