期刊
FREE RADICAL RESEARCH
卷 36, 期 11, 页码 1147-1153出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/1071576021000016409
关键词
PKC delta; Ca2+; p53; H2O2; apoptosis; endothelial cells
To clarify the signaling pathways of oxidative stress-induced apoptosis in bovine aortic endothelial cells (BAEC), we treated cells with 1 mM H2O2 and investigated the roles of protein kinase C delta (PKCdelta) and Ca2+ in the accumulation of p53 associated with apoptosis. The treatment of cells with H2O2 caused the accumulation of p53, which was inhibited by rottlerin (a PKCdelta inhibitor) but not by BAPTA-AM (an intracellular Ca2+ chelator). PKCdelta itself was activated through the phosphorylation at tyrosine residues. H2O2 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 PKCdelta contributes to the accumulation of p53 and that Ca2+ plays a role in downstream signals of p53 leading to apoptosis in H2O2-treated BAEC.
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