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. 2004 Aug 1;18(15):1824–1837. doi: 10.1101/gad.1223504

Figure 4.

Figure 4.

PKC δ mediated the enhanced response of c-abl-/- osteoblasts. (A) Enforced expression of PKC δ in normal osteoblasts made the cells more sensitive to arsenate-induced Prx I expression. Normal osteoblasts were infected with retroviruses expressing GFP or PKC δ, selected against hygromycin for 7 d with medium changed every 2 d, and challenged with arsenate, and Prx I induction was analyzed with Northern blot. (B) Quantitation data from three experiments. (C) Overexpression of PKC δ led to increased cell death following arsenate treatment. The experiment was carried out as described in Figure 1G. (D) Induction of Prx I in both abl-/- and wild-type control osteoblasts could be inhibited by Rottlerin treatment. Cells were pretreated with rottlerin for 1 h before the addition of arsenate. Prx I mRNA levels were determined by Northern blot. Fold induction was calculated by comparing to the basal level of Prx I in untreated cells. (E) Arsenate-induced Nrf2 accumulation was blocked by inhibition of PKC δ with rottlerin. (F) Arsenate-induced cell death in abl-/- osteoblasts was rescued by rottlerin. abl-/- osteoblasts were pretreated with 5 μM rottlerin for 1 h before arsenate was added to the final concentrations of 0.10 or 0.125 mM. Cell death rates were determined after 20-h treatments.