Skip to main content
. 2019 Sep 25;9(24):7268–7281. doi: 10.7150/thno.33006

Figure 6.

Figure 6

Maf1 ameliorates cardiac hypertrophy via negative regulation of RNA pol III transcription. The experiments were all carried out in primary cardiomyocytes of SD rats. The cardiomyocytes were treated with 50 μM PE for 24 hours. (A) The effects of Maf1 knockdown and pol III inhibition on ANP mRNA expression was determined by q-PCR, and GAPDH was used as an internal control; n=6. (B) The effects of Maf1 knockdown and pol III inhibition on cell surface areas; n=3. (C) Cardiomyocytes were stained for troponin I expression, and the nuclei were stained with DAPI. (D) Puromycin labeling to measure protein synthesis during si-Maf1-mediated cardiac hypertrophy and the effect of the pol III inhibitor on protein synthesis. (E) Puromycin labeling to measure protein synthesis in Ad-Maf1-regulated cardiac hypertrophy, and the effect of pol III inhibitor on protein synthesis. One micromolar puromycin was added in each well and incubated for 30 minutes. Cardiomyocytes were then collected and subjected to WB analysis. Coomassie blue was used as an internal control. **p<0.01 versus the corresponding control group. NS indicates no significant difference versus the corresponding control group.