Ectopic expression of BcI-2, but not BcI-xL rescues Ramos B cells from Fas-mediated apoptosis
✍ Scribed by Mohammad K. Alam; Stephen Davison; Nisha Siddiqui; John D. Norton; John J. Murphy
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 617 KB
- Volume
- 27
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
The human Burkitt lymphoma Ramos B cell line can be induced to undergo apoptosis in response to a variety of different agents, including calcium ionophores, anti-immunoglobulin (lg) and macromolecular synthesis inhibitors. In addition, following up-regulation of the Fas (CD95) surface receptor by CD40 ligation, these cells also become susceptible to apoptosis induction by Fas ligation. We have previously shown that protection from calcium ionophoreand macromolecular synthesis inhibitor-induced apoptosis by CD40 ligation is associated with a rapid up-regulation of Bcl-xL followed by a more moderate and delayed up-regulation of Bcl-2. We show here that overexpression of BcI-xL, like Bcl-2, protects Ramos cells from apoptosis induction in response to calcium ionophore, anti-lg and macromolecular synthesis inhibition. However, in contrast to Bcl-2, ectopic overexpression of BcI-xL does not rescue from Fas-mediated apoptosis. Thus, in Ramos B cells, the Fas apoptotic pathway exhibits differential sensitivity to inhibition by Bcl-2 family members. These findings also suggest that CD40 signaling provides a switch which renders the cells susceptible to Fasligand mediated apoptosis through up-regulation of Fas whilst affording protection from