Table 1

The PKC activator PMA, but not the inactive PMA derivative 4αPMA, promote apoptosis in ara-C–treated cells

Annexin V/PIReduced ΔΨm
U937/neoU937/Bcl-2ΔU937/neoU937/Bcl-2Δ
% apoptotic cells % cells
Control2.5  ± 0.22.0  ± 0.18.5  ± 0.25.4  ± 0.2
PMA8.5  ± 0.25.0  ± 0.623.4  ± 2.214.2  ± 0.6
ara-C30.4  ± 1.29.5  ± 0.236.5  ± 1.29.5  ± 0.9
ara-C+PMA59.5  ± 1.61-150 44.6  ± 0.81-160 63.1  ± 2.01-150 34.7  ± 0.81-160
4αPMA7.5  ± 0.94.3  ± 0.612.4  ± 0.57.0  ± 0.6
ara-C+4αPMA29.7  ± 1.18.6  ± 0.432.3  ± 0.813.5  ± 1.1

U937/neo and U937/Bcl-2Δ cells were exposed to ara-C (0.5 μM) with or without PMA (10 nM) or an inactive phorbol control (4α-PMA; 10 nM) for 24 hours. Values represent the means for triplicate experiments (± S.D.) and are expressed as the percentage of apoptotic cells determined by Annexin V and propidium iodide, or the percentage of cells exhibiting low levels of DiOC6 uptake, reflecting loss of Δ Ψ m.

    • ↵1-150 , P < 0.05, significantly greater than values for ara-C alone.

    • ↵1-160 , P > 0.05, not significantly different from values for ara-C alone in empty-vector controls.