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HSP25 inhibits radiation-induced apoptosis through reduction of PKCδ-mediated ROS production
- HSP25 inhibits radiation-induced apoptosis through reduction of PKCδ-mediated ROS production
- Lee Y.-J.; Lee D.-H.; Cho C.-K.; Chung H.-Y.; Bae S.; Jhon G.-J.; Soh J.-W.; Jeoung D.-I.; Lee S.-J.; Lee Y.-S.
- Ewha Authors
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- Oncogene vol. 24, no. 23, pp. 3715 - 3725
- SCI; SCIE; SCOPUS
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- Since radiation-induced caspase-dependent apoptosis and ROS generation were partially prevented by HSP25 overexpression, similar to the treatment of control cells with antioxidant agents such as DPI and tiron, questions arise whether radiation-mediated ROS generation contributes to the apoptotic cell death, and also whether HSP25 overexpression can reduce ROS mediated apoptotic cell death. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. When HSP25 was overexpressed, effects similar to the treatment of cells with the antioxidants were obtained, indicating that HSP25 suppressed radiation-induced mitochondrial alteration that resulted in apoptosis. Furthermore, activation of p38 MAP kinase by radiation was associated with radiation-induced cell death and ROS production and PKCδ was an upstream molecule for p38 MAP kinase activation, ROS generation and subsequent caspase-dependent apoptotic events. However, in the HSP25 overexpressed cells, the above-described effects were blocked. In fact, radiation-induced membrane translocation of PKCδ and tyrosine phosphorylation were inhibited by HSP25. Based on the above data, we suggest that HSP25 downregulates PKCδ, which is a key molecule for radiation-induced ROS generation and mitochondrial-mediated caspase-dependent apoptotic events. © 2005 Nature Publishing Group All rights reserved.
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