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

Uhrf1 promotes the expression of mTOR in MIRI. (A) The relative mRNA expressions of mTOR in Myocardial ischemia-reperfusion model in vitro were determined by qRT-PCR. (B) Western blot was used to detect the expression level of mTOR protein in each group. GAPDH serves as a loading control. (C) Expression of mTOR protein relative to GAPDH data from 3 biological repeats is shown. (D) Detection of mTOR protein expression and semi quantitative analysis by immunofluorescence microscopy (x200). Scale bar, 100μm. 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 5. Uhrf1 promotes the expression of mTOR in MIRI. (A) The relative mRNA expressions of mTOR in Myocardial ischemia-reperfusion model in vitro were determined by qRT-PCR. (B) Western blot was used to detect the expression level of mTOR protein in each group. GAPDH serves as a loading control. (C) Expression of mTOR protein relative to GAPDH data from 3 biological repeats is shown. (D) Detection of mTOR protein expression and semi quantitative analysis by immunofluorescence microscopy (x200). Scale bar, 100μm. 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.