Research Paper Volume 14, Issue 4 pp 1678—1690

Figure 3. Upregulation of Bcl-2 by Cr(VI) was via increasing its stability and depends upon PKC. (A) Cells were exposed to Cr(VI) for 2 h and 1 month and their sensitivities to doxorubicin (5 μM)-induced apoptosis were analyzed by DNA fragmentation assay. The error bars were SD (n = 5, p < 0.01). (B) BEAS-2B cells were transiently or persistently exposed to Cr(VI) prior to doxorubicin treatment, and then examined for Bcl-2 expression. Actin was the loading control. (C) After the treatments as described above, Bax expression was analyzed. Actin was the loading control. (D) After adding GO6976, Bcl-2 expression in the cells received the treatments as described above was tested by immunoblotting. Actin was the loading control. (E) Cells chronically exposed to Cr(VI) were treated with doxorubicin or co-treated with GO6976, prior adding CHX (0.5 μM). Bcl-2 expression was then analyzed at different time points of CHX block. Actin was the loading control. (F) Cells chronically exposed to Cr(VI) were treated with doxorubicin. Afterwards, actinomycin D (ATC, 1.0 nM) was added and expression levels of bcl-2 gene were analyzed at different time points of ATC block by real time PCR. The error bars were SD (n = 5, p < 0.05).