Fig. 3: MIAT is inhibited by BACH2 in adult human cardiac fibroblasts and human cardiomyocytes, and cardiac BACH2 genes are downregulated in failing human and mouse hearts.

Primary adult human cardiac fibroblasts (HCFs) (A, B) and AC-16 cardiomyocytes (C, D) were transfected with control scramble siRNA (si-control) or BACH2 siRNA (si-BACH2). HCFs (E, F) and AC-16 cardiomyocytes (G, H) were infected with control adenovirus (Ad-GFP) or adenovirus expressing human BACH2 (Ad-hBACH2). QRT-PCR analyses for BACH2 (A, C, E, G) or MIAT (B, D, F, H) were then performed to check their expression after the indicated transfection or infection. Data were normalized to GAPDH and are expressed relative to controls. N = 6 per group. Unpaired 2-tailed t-test. *P < 0.01, **P < 0.05, or ***P < 0.001 vs. control: either si-control or Ad-GFP control. Data are presented as the mean ± SEM. I QRT-PCR expression analysis of BACH2 in left ventricles from patients with heart failure with reduced ejection fraction (HFrEF) relative to non-failing heart tissues. N = 6 per group. Unpaired 2-tailed t-test. *P < 0.01 vs. non-failing control. J QRT-PCR expression analysis of Bach2 in infarcted area at 2 weeks after MI relative to sham controls. N = 6 per group. Unpaired 2-tailed t-test. ***P < 0.001 vs. sham control. Data are presented as the mean ± SEM.