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. 2013 Sep 16;110(40):16127–16132. doi: 10.1073/pnas.1311055110

Fig. 2.

Fig. 2.

Cenersen reduces p53 and PUMA expression in RPS14-deficient erythroblasts and decreases apoptosis. Cenersen treatment resulted in significant down-regulation of p53 (A) and its downstream target PUMA (B) in RPS14-deficient erythroblasts compared with control oligonucleotide-treated cells. Cenersen, black bars; control oligonucleotide, open bars. Expression levels are shown as means ± SEM of fluorescence intensity (n = 8). Representative photomicrographs are shown of p53 (C) and PUMA (D) immunofluorescence in RPS14-deficient erythroblasts that have undergone cenersen (Right) or control oligonucleotide treatment (Left), with p53 staining shown in green, PUMA staining in red, and DAPI in blue (magnification, ×630). (E) Percentage apoptosis as assessed by Annexin V-positive staining, shown as means ± SEM (n = 10). Cenersen, black bars; control oligonucleotide, open bars. (F) Representative flow cytometry contour plots showing a significant increase in the viable, nonapoptotic (Annexin V-negative, propidium iodide-negative) cell population in RPS14-deficient erythroblasts after cenersen treatment. P values were calculated by Wilcoxon signed-rank test: *P < 0.05; **P < 0.01.