Abstract
Apoptosis is a process whereby developmental or environmental stimuli activate a genetic programme to execute a specific series of events that culminate in the death and efficient disposal of a cell. Although a series of recent data suggested that neuronal death following cerebral ischemia occurs through an apoptotic pathway, additional work is needed to establish the existence of a causal relationship between gene expression and DNA breaks in neuronal death. We investigate the role of p53 and Bax proteins in the induction of apoptosis induced by a new transient focal ischemia model in the rat pup. Our results show that wild-type p53 exerts a significant and time-dependent effect in the initiation of apoptosis, and that apoptosis is induced via DNA-strand breakage. Subsequently, increased Bax expression was observed in the cytoplasm of dying cells located in the infarct, whereas an increased Bcl-2 and hsp72 staining was detectable in survival cells and reactive glia present at the periphery of the lesion.
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Renolleau, S., Benjelloun, N., Ben-Ari, Y. et al. Regulation of apoptosis-associated proteins in cell death following transient focal ischemia in rat pups. Apoptosis 2, 368–376 (1997). https://doi.org/10.1023/A:1026453623753
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DOI: https://doi.org/10.1023/A:1026453623753