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. 2021 Sep 2;10(17):e020895. doi: 10.1161/JAHA.121.020895

Figure 3. Role of p53 in apoptosis induced by PHD (prolyl hydroxylase domain) inhibition using CoCl2 in cultured rat cardiomyocytes.

Figure 3

A, Tp53 expression in cultured cardiomyocytes, treated with vehicle (Veh) and CoCl2 (500 μmol/L) for 24 hours, or transfected with small interfering RNA (siRNA) for control (CTL) (scramble siRNA, CTL) and p53, was quantified by quantitative reverse transcription‐polymerase chain reaction; n=6 in each group. B, Expression of Hif‐1α, p53, and CC‐3 (cleaved caspase 3) in cardiomyocytes treated with Veh and CoCl2 (500 μmol/L) for 24 hours, or transfected with siRNA for CTL (scramble siRNA, CTL) and p53. GAPDH (glyceraldehyde 3‐phosphate dehydrogenase) was used as a loading CTL. C, Quantification of Western blots shown in (B); n=6 in each group. Data are shown as a ratio to the average of Veh+CTL. D, Images of cardiomyocytes treated with Veh and CoCl2 (500 μmol/L), or transfected with siRNA for CTL (scramble siRNA, CTL) and p53. E, Cellular viability using cultured cardiomyocytes treated with Veh and CoCl2 (500 μmol/L), or transfected with siRNA for CTL (scramble siRNA, CTL) and p53 by CellTiterBlue Assay; n=6 in each group. **P<0.01, analyzed by 1‐way ANOVA, followed by Tukey post hoc test. KD indicates knockdown; and N/A, not applicable.