Roles of p53, c-Myc, Bcl-2, Bax and caspases in serum deprivation-induced neuronal apoptosis: a possible neuroprotective mechanism of basic fibroblast growth factor.

Using flow cytometric analysis, we examined the temporal changes of p53, c-Myc, Bcl-2, Bax expression in rat primary cortex neurons after serum deprivation. Activities of caspase-1 and caspase-3 were also measured. Serum deprivation induced apoptosis accompanied by a rapid down-regulation of p53, Bcl-2 and an up-regulation of c-Myc, Bax and caspase-3 activity. Pretreatment with basic fibroblast growth factor prevented the apoptosis with an attenuation of the changes of p53, Bcl-2, Bax levels and caspase-3 activity but had no effect on the change of c-Myc level. These results suggest that serum deprivation induces apoptosis through a signaling pathway involving p53, Bcl-2, Bax, c-Myc and caspase-3. The effect of the basic fibroblast growth factor against apoptosis may result from its capability of blocking the apoptosis cascade.