Fig 2: Effect of Maf1 knockout on AB-induced hypertrophy. The experiments were all carried out in mice. (A) Western blots showing Maf1 and vinculin expression in mouse hearts. Vinculin was used as an internal control. (B) Images of whole hearts from Maf1 knockout mice at 4 weeks after sham or AB surgery. (C-D) The heart or lung/body weight ratios were determined and showed that knockout of Maf1 could exacerbate AB-induced hypertrophy and pulmonary edema; WT+Sham n=7; MKO+Sham n=7; WT+AB n=8; MKO+AB n=6. (G) The effect of Maf1 knockout on ANP mRNA expression was determined by q-PCR, and GAPDH was used as an internal control; n=4-8. (E-F) Images of H&E-stained heart sections from mice at 4 weeks after sham or AB surgery; n=3. (H-K) The effects of Maf1 knockout on echocardiographic parameters (EF, LVEDd, LVEDs and LVPWd). *p<0.05 versus the corresponding control group. **p<0.01 versus the corresponding control group. NS indicates no significant difference versus the corresponding control group.

Fig 3: Maf1-mediated cardiac hypertrophy is related to RNA polymerase III transcription. The experiments in Figure 5A-D were carried out in mice, while other experiments were carried out in primary cardiomyocytes of SD rats. (A) Expression levels of the relevant products of RNA pol III transcription 5SrRNA and tRNALeu and the pol III subunit Brf1 were detected by q-PCR at 2 and 4 weeks after surgery, and ARPP P0 was used as an internal control; n=5-7.(B-D) Expression levels of the relevant products of RNA pol III transcription 5SrRNA and tRNALeu and the pol III subunit Brf1 were detected by q-PCR at 4 weeks after sham or AB surgery; n=4-6. (E-G) The cardiomyocytes were treated with 50 µM PE for 24 hours. Expression levels of the relevant products of RNA pol III transcription 5SrRNA and tRNALeu and the pol III subunit Brf1 were detected by q-PCR after PE treatment; n=6. *p<0.05 versus the corresponding control group. **p<0.01 versus the corresponding control group.

Fig 4: Effect of Maf1 upregulation on AB-induced hypertrophy. The experiments were all carried out in mice. (A-B) Western blots showing Maf1 and vinculin expression in mouse hearts, and the quantitative analysis of those blots. Vinculin was used as an internal control; n=3. (C) Images of whole hearts from Maf1-overexpressing mice 4 weeks after sham or AB surgery. (D-E) The heart or lung/body weight ratio was detected and showed that upregulation of Maf1 expression could attenuate AB-induced hypertrophy and pulmonary edema; Ad-GFP+Sham n=7; Ad-Maf1+Sham n=7; Ad-GFP +AB n=6; Ad-Maf1+AB n=5. (F-J) The effects of Maf1 upregulation on echocardiographic parameters (EF, LVEDd, LVEDs and LVPWd). (J) The effect of Maf1 upregulation on ANP mRNA expression was determined by q-PCR, and GAPDH was used as an internal control; n=4-5. (K-L) Images of H&E-stained heart sections from mice at 4 weeks after sham or AB surgery; n=3. *p<0.05 versus the corresponding control group. **p<0.01 versus the corresponding control group.

Fig 5: Effect of AB on Maf1 expression in cardiomyocytes and the genomic sequence of Maf1 knockout mice. The experiments in Figure 1A-D and Figure 1F-G were carried out in mice, while other experiments were carried out in primary cardiomyocytes and cardiac fibroblasts of SD rats. (A-B) Western blots showing total Maf1 and total vinculin expression in mouse hearts at 4 weeks after sham or AB surgery, and the quantitative analysis of those blots; n=6. (C-D) Western blots showing nuclear Maf1 and nuclear vinculin expression in mouse hearts at 4 weeks after sham or AB surgery, and the quantitative analysis of those blots. Vinculin was used as an internal control; n=3. (E) The cardiomyocytes were treated with 50 µM PE for 24 hours. Cardiomyocytes were stained with troponin I, the nuclei were stained with DAPI, and Maf1 was stained with a special antibody. (F-G) Maf1 deficiency was identified through genetic sequencing, and 13 bases of Maf1 were deleted. *p<0.05 versus the corresponding control group. **p<0.01 versus the corresponding control group.