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Murine thymic lymphoma cells and 3SBH5 are quite sensitive to X-rays and undergo apoptosis shortly after X-irradiation. Phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), blocked the radiation-induced apoptosis in the 3SBH5 cells. On the other hand, chelerythrine, a PKC inhibitor, enhanced the radiation-induced apoptosis. These results suggest that PKC plays a key role in the regulation of radiation-induced apoptosis in 3SBH5 cells. Irradiation alone had no effect on the distribution of PKC subtypes (alpha, betaI, betaII and delta) in the 3SBH5 cells. The amounts of PKC beta I in the cytosol of the 3SBH5 cells decreased in the cells pretreated with PMA. Irradiation did not change the decrease of PKC beta I. In contrast, treatment with PMA had no effect on the distribution of the other PKC subtypes. PMA appears to influence processes of radiation-induced apoptosis through the change in the distribution of PKC beta I. In addition, it was demonstrated that immunoprecipitates by anti-PKC alpha antibody included Raf-1, one of stress response proteins, in 3SBH5 cells after irradiation. These results suggest that PKC alpha might participate as a regulator in radiation-induced apoptsis, but PKC beta I might influence the apoptosis indirectly through the PMA-induced change of the distribution. |
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