Roles of protein kinase C delta in the accumulation of P53 and the induction of apoptosis in H2O2-treated bovine endothelial cells |
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Authors: | Niwa Koichi Inanami Osamu Yamamori Tohru Ohta Toshio Hamasu Taku Karino Takeshi Kuwabara Mikinori |
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Affiliation: | a Laboratory of Biofluid Dynamics, Research Institute for Electronic Science, Hokkaido University, Sapporo 060-0812, Japan.b Laboratory of Radiation Biology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.c Laboratory of Pharmacology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan. |
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Abstract: | To clarify the signaling pathways of oxidative stress-induced apoptosis in bovine aortic endothelial cells (BAEC), we treated cells with 1 mM H 2 O 2 and investigated the roles of protein kinase C δ(PKC δ) and Ca 2+ in the accumulation of p53 associated with apoptosis. The treatment of cells with H 2 O 2 caused the accumulation of p53, which was inhibited by rottlerin (a PKC δinhibitor) but not by BAPTA-AM (an intracellular Ca 2+ chelator). PKC δitself was activated through the phosphorylation at tyrosine residues. H 2 O 2 induced the release of cytochrome c and the activation of caspases 3 and 9, and these apoptotic signals were inhibited by rottlerin and BAPTA-AM. These results suggest that PKC δcontributes to the accumulation of p53 and that Ca 2+ plays a role in downstream signals of p53 leading to apoptosis in H 2 O 2 -treated BAEC. |
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Keywords: | Pkcδ Ca 2 P53 H 2 O 2 Apoptosis Endothelial Cells |
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