Fig. 6.
Fig. 6. The ability of BRY to potentiate LC-induced apoptosis is PKC dependent. / (A) U937 cells were either pretreated or posttreated with the specific PKC inhibitor bisindolylmaleimide I (GF109203X; 1 μM), as indicated. Cells were subjected to cytocentrifugation at 24 hours and the extent of apoptosis was determined by morphologic analysis. [o] indicates the extent of cell death observed in cells treated with LC alone and [*] indicates the extent observed in LC/B-treated cells. Values represent the means for triplicate experiments (± SEM). (B) U937 cells were exposed to either media (C), BRY (10 nM) (B), LC (1 μM) or the LC/BRY combination (LC/B) for 24 hours. The amount of phorbol-activated PKC activity remaining was then determined. Values represent the means for triplicate experiments (± SEM). (C) Western blots of PKC isoform expression (PKCα, PKCβI, and PKCβII) at the indicated intervals following drug exposure.

The ability of BRY to potentiate LC-induced apoptosis is PKC dependent.

(A) U937 cells were either pretreated or posttreated with the specific PKC inhibitor bisindolylmaleimide I (GF109203X; 1 μM), as indicated. Cells were subjected to cytocentrifugation at 24 hours and the extent of apoptosis was determined by morphologic analysis. [o] indicates the extent of cell death observed in cells treated with LC alone and [*] indicates the extent observed in LC/B-treated cells. Values represent the means for triplicate experiments (± SEM). (B) U937 cells were exposed to either media (C), BRY (10 nM) (B), LC (1 μM) or the LC/BRY combination (LC/B) for 24 hours. The amount of phorbol-activated PKC activity remaining was then determined. Values represent the means for triplicate experiments (± SEM). (C) Western blots of PKC isoform expression (PKCα, PKCβI, and PKCβII) at the indicated intervals following drug exposure.

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