Down-regulation of bcl-xs gene expression in rat thymocytes by dexamethasone

In order to test a hypothesis that the expression of bcl-x gene promotes apoptosis by antagonizing the function of bcl-2 gene product, time course of the expression of bcl-x was investigated using the dexamethasone-treated rat thymocytes which were undergoing apoptosis. Unexpectedly, dexamethasone suppressed the expression of bcl-x in a dose- and time-dependent manner. Such decrease was detected even in the presence of cycloheximide, suggesting that the suppression is due to the genomic (primary) effect of dexamethasone. Since the expression of bcl-xL, as measured by a specific nucleotide probe, was not detected at a quantifiable level, the decrease was apparently attributed to that in bcl-xS. Our present observations propose a new role of the bcl-xS gene product, in which the bcl-x gene product may be necessary for survival of immature thymocytes rather than for their apoptosis.