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KMID : 1161520000040030279
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Animal Cells and Systems
2000 Volume.4 No. 3 p.279 ~ p.285
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Activation of PKC-βII is required for vitamin e-succinate-induced apoptosis of U937 cells
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Kim Song-Ja
Park Jae-Han
Lee Sun-Ryung
Bang Ok-Sun
Kang Shin-Sung
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Abstract
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Vitamin E?succinate (VES) treatment of U937 human monoblasts induced cells to undergo apoptosis. After 96 h of VES treatment at 10μg/ml, more than 80% of cells appeared apoptotic. Evidence for apoptosis by VES was based on propidium iodide staining for detection of chromatin condensational fragmentation and electrophoretic DNA ladder formation. Western blot analyses showed a transient increase in Fas and p21 protein levels up to 48 h after the VES treatment. Protein expression and activity of CDK1 and lamin B degradation were remarkably induced by VES, following the cleavage of caspase?3 after 48 h. The VES?induced apoptosis was found to involve activation of PKC as shown by increases in membrane translocation of PKCPII and PKC activity. Pretreatment of GF109203X (PKC inhibitor) prior to VES treatment almost completely inhibited the induction of apoptosis as assessed by blockage of VES?induced caspase?3 activity and DNA fragmentation. However, GF109203X had no effect on the VES?induced nitric oxide synthesis, which was required for monocytic differentiation in our previous report (J Cell Sci 111, 435, 1998). Taken together, our data suggest that induction of apoptosis by VES in U937 cells occurs through activation of PKC?βII resulting in the activation of caspase?3 cascade and is independent of nitric oxide.
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KEYWORD
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Apoptosis, Caspase, Fas, PKC, Vitamin E-succinate
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