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

Authors
Citation
X. Liu et Xz. Zhu, 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, NEUROREPORT, 10(14), 1999, pp. 3087-3091
Citations number
24
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROREPORT
ISSN journal
0959-4965 → ACNP
Volume
10
Issue
14
Year of publication
1999
Pages
3087 - 3091
Database
ISI
SICI code
0959-4965(19990929)10:14<3087:ROPCBB>2.0.ZU;2-O
Abstract
USING flow cytometric analysis, we examined the temporal changes of p53, c- Myc, Bcl-2, Bar expression in: rat:primary cortex neurons after serum depri vation. Activities of:caspase-1 and caspase-3 were also measured. Serum dep rivation induced apoptosis accompanied by a:rapid down-regulation of p53, B cl-2 and an up-regulation of c-Myc, Bar and caspase-3 activity. Pretreatmen t with basic fibroblast growth factor prevented the apoptosis:with an atten uation of the changes of p53, Bcl-2, Bar levels and caspase-3 activity but had no effect on the change of c-Myc level. These results suggest that seru m deprivation induces apoptosis through a signaling pathwat 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 apo ptosis cascade. (C) 1999 Lippincott Williams & Wilkins.