Abstract
In the context of genetic control over cell death in brain following ischemia, we studied the functional significance of the newly described caspase-3 member of the interleukin-converting enzyme (ICE) protease family. At both message and protein levels, this gene’s product was upregulated in selectively vulnerable regions following ischemia. Coincident with cell death, the precursor protein was proteolytically cleaved and the protease activity increased. In regions of neuronal death, PARP cleavage was demonstrated. Inhibition of caspase-3 protease activity decreased both neuronal death and deoxyribonucleic acid (DNA) fragmentation (TUNEL labeling) and increased survival in selectively vulnerable brain regions 1 week after ischemia. These data support the view that caspase-3 protease is an inducible modulator of cell death in ischemic brain.
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