Figure 6. Independent regulation of p53 and PKCδ during cisplatin nephrotoxicity.

(A) Cisplatin-induced p53 activation in kidney tissues. Wild-type and Pkcd^–/– mice were injected with 30 mg/kg cisplatin before collection of whole kidney lysates for immunoblotting. (B) Cisplatin-induced p53 activation in primary Pkcd^–/– kidney tubular cells. The cells were incubated with 50 μM cisplatin for 24 hours to collect lysate for immunoblotting. (C) Cisplatin-induced PKCδ activation in kidney tissues. Wild-type and p53^–/– mice were injected with 30 mg/kg cisplatin before collection of whole kidney lysates for immunoblotting. (D) Cisplatin-induced PKCδ activation in primary p53^–/– kidney tubular cells. The cells were incubated for 24 hours with 50 μM cisplatin to collect lysate for immunoblotting. (E) Effects of pifithrin-α and rottlerin on cisplatin-induced apoptosis in primary Pkcd^–/– kidney tubular cells. The cells were treated for 24 hours with 50 μM cisplatin in the absence or presence of 10 μM rottlerin or 20 μM pifithrin-α to determine the percentage of apoptosis by morphological methods. (F) Effects of pifithrin-α and rottlerin on cisplatin-induced apoptosis in primary wild-type and p53^–/– kidney tubular cells. The cells were treated for 24 hours with 50 μM cisplatin in the absence or presence of 10 μM rottlerin or 20 μM pifithrin-α to determine the percentage of apoptosis by morphological methods. Mean ± SD, n = 4. ^#P < 0.05 versus the cisplatin group of the same genotype cells.