INVOLVEMENT OF CD45 IN DEXAMETHASONE-INDUCED AND HEAT-SHOCK-INDUCED APOPTOSIS OF RAT THYMOCYTES

Citation
L. Troiano et al., INVOLVEMENT OF CD45 IN DEXAMETHASONE-INDUCED AND HEAT-SHOCK-INDUCED APOPTOSIS OF RAT THYMOCYTES, Biochemical and biophysical research communications, 214(3), 1995, pp. 941-948
Citations number
37
Categorie Soggetti
Biology,Biophysics
ISSN journal
0006291X
Volume
214
Issue
3
Year of publication
1995
Pages
941 - 948
Database
ISI
SICI code
0006-291X(1995)214:3<941:IOCIDA>2.0.ZU;2-P
Abstract
CD45 is a transmembrane tyrosine-specific phosphatase which participat es in lymphoid cell signal transduction during T cell activation, as w ell as in intrathymic negative and positive selection. In mammals, thi s molecule exhibits a variety of isoforms of different molecular weigh t, whose roles have still to be fully elucidated. We report here that apoptosis of rat thymocytes after in vitro dexamethasone and heat shoc k treatment was accompanied by an early significative increase of cell s expressing CD45RC, the high molecular weight isoform of CD45 molecul e. The same phenomenon was observed in thymocytes derived from irt viv o dexamethasone-treated rats. However, the increase of CD45RC(+) cells was not apparently characteristic of cells undergoing apoptosis, as t he same phenomenon was also observed in rat thymocytes induced to prol iferate by Concanavalin A. On the whole, these results suggest that CD 45 modulation can be added to the list of early molecular events, such as the increased expression of genes (ornithine decarboxylase), proto -oncogenes (c-fos, c-jun, c-myc) and activation of transcription facto rs (AP-I, NFkB), we previously demonstrated in the same experimental m odel to occur and to be shared by these two apparently opposite biolog ical processes, i.e.,cell proliferation and apoptosis, both likely dep ending on a complex balance of protein phosphorylation and dephosphory lation. (C) 1995 Academic Press. Inc.