Opposing effects of protein kinase C δ and protein kinase B α on H2O2-induced apoptosis in CHO cells

H2O2-induced apoptosis was enhanced in the CHO cell line overproducing protein kinase C delta (PKC delta) as judged by DNA fragmentation. In response to the H2O2 treatment, PKC delta was tyrosine phosphorylated and recovered as a constitutively active form, but its proteolytic fragment was not generated. In contrast, H2O2-induced apoptosis was suppressed in the CHO cell line overexpressing protein kinase B alpha (PKB alpha). Consistently, phosphorylation of BAD, a pro-apoptotic protein negatively regulated by PKB alpha, was sustained in the cells overproducing PKB alpha, but was not changed in the cells overexpressing PKC delta. In the CHO cell line overproducing both PKC delta and PKB alpha, H2O2-induced tyrosine phosphorylation of PKC delta was suppressed, and DNA fragmentation was diminished concomitantly. These results suggest that PKC delta contributes to H2O2-induced apoptosis by a mechanism independent of BAD and that PKC delta is a target of PKB for the regulation of cell survival. (C) 1999 Academic Press.