p53 activation inhibits ochratoxin A-induced apoptosis in monkey and human kidney epithelial cells via suppression of JNK activation

► Monkey and human kidney epithelial cells were used to investigate the role of p53 in ochratoxin A-induced apoptosis. ► Ochratoxin A was capable of inducing p53 activation in all cell lines tested. ► Inhibition of p53 activation promoted apoptosis induction by ochratoxin A. ► Pro-survival activity of p53 was attributed to its ability to suppress JNK activation. Ochratoxin A (OTA), one of the major food-borne mycotoxins, induces apoptosis in various types of cells. Induction of apoptosis is suggested to be one of the major cellular mechanisms behind OTA-induced diverse toxic effects. However, the molecular mechanisms involved, especially the role of p53 in OTA-induced apoptosis have not been clearly elucidated. In the present study, we find that p53 activation exerts pro-survival function to inhibit apoptosis induction in MARC-145, Vero monkey kidney cells and HEK293 human kidney cells in response to ochratoxin A treatment. We further demonstrate that the pro-survival activity of p53 is attributed to its ability to suppress JNK activation that mediates apoptotic signaling through down-regulation of Bcl-xL. To our knowledge, this is first report of pro-survival role of p53 in OTA-induced apoptosis in kidney epithelial cells. Our findings provide a novel insight into the mechanisms of OTA-induced apoptosis in kidney epithelial cells.