Research Paper Volume 13, Issue 7 pp 9704—9718

Uhrf1 regulates H3K9me2 modification of mTOR to inhibit the effect of autophagy in myocardial ischemia-reperfusion injury

The effect of Uhrf1 on cardiomyocyte apoptosis during myocardial ischemia-reperfusion injury. (A) The relative mRNA expressions of Bax, Bcl-2 and Caspase-3 in myocardial ischemia-reperfusion model in vitro were determined by qRT-PCR. (B) Western blot was used to detect the expression level of Bax, Bcl-2 and Caspase-3 protein in each group. GAPDH serves as a loading control. (C) Expression of Bax, Bcl-2 and Caspase-3 protein relative to GAPDH data from 3 biological repeats is shown. (D) Detection of Bax, Bcl-2 and Caspase-3 protein expression and semi quantitative analysis by immunofluorescence microscopy (x200). Scale bar, 100 μm. Data shown are mean ± SD. *P P P P in vitro oxidative stress model; NC, negative control of RNAi; si, RNAi knockdown of Uhrf1; Uhrf1, Uhrf1 overexpression.

Figure 3. The effect of Uhrf1 on cardiomyocyte apoptosis during myocardial ischemia-reperfusion injury. (A) The relative mRNA expressions of Bax, Bcl-2 and Caspase-3 in myocardial ischemia-reperfusion model in vitro were determined by qRT-PCR. (B) Western blot was used to detect the expression level of Bax, Bcl-2 and Caspase-3 protein in each group. GAPDH serves as a loading control. (C) Expression of Bax, Bcl-2 and Caspase-3 protein relative to GAPDH data from 3 biological repeats is shown. (D) Detection of Bax, Bcl-2 and Caspase-3 protein expression and semi quantitative analysis by immunofluorescence microscopy (x200). Scale bar, 100 μm. Data shown are mean ± SD. *P < 0.05, **P <0.01, ***P <0.001, ****P < 0.0001. N=3 per group. Model, in vitro oxidative stress model; NC, negative control of RNAi; si, RNAi knockdown of Uhrf1; Uhrf1, Uhrf1 overexpression.