Cytoplasmic acidification is not an effector mechanism of VP16 or DEX-induced apoptosis in CEM T leukaemia cells

Citation
Rsp. Benson et al., Cytoplasmic acidification is not an effector mechanism of VP16 or DEX-induced apoptosis in CEM T leukaemia cells, J CELL SCI, 112(11), 1999, pp. 1755-1760
Citations number
39
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF CELL SCIENCE
ISSN journal
00219533 → ACNP
Volume
112
Issue
11
Year of publication
1999
Pages
1755 - 1760
Database
ISI
SICI code
0021-9533(199906)112:11<1755:CAINAE>2.0.ZU;2-6
Abstract
The role of intracellular acidification in the execution phase of apoptosis is not well understood. Here we examine the effect of Bcl-2 over-expressio n on intracellular acidification occurring during apoptosis. We found, that in CEM cells, neither DEX nor VP16-induced apoptosis lead to a significant change in intracellular pH (pH(i)). Furthermore, we found that shifting pH i away from physiological values was unable to induce chromatin condensatio n or poly(ADP-ribose) polymerase (PARP) cleavage in the presence of Bcl-2 o ver-expression. However, it was found that maximum chromatin condensation a nd PARP cleavage occurred at near physiological pHi values. Taken together these data suggest that intracellular acidification does not trigger the ef fector phase of CEM apoptosis.