Fig. 4: BACH2 genes are upregulated in mouse left ventricles, human cardiac fibroblasts, and human and rodent cardiomyocytes by carvedilol. | Cell Death Discovery

Fig. 4: BACH2 genes are upregulated in mouse left ventricles, human cardiac fibroblasts, and human and rodent cardiomyocytes by carvedilol.

From: BACH2 links β1-adrenergic receptor/β-arrestin1 signaling to MIAT to inhibit cardiac fibroblast activation and cardiomyocyte apoptosis

Fig. 4: BACH2 genes are upregulated in mouse left ventricles, human cardiac fibroblasts, and human and rodent cardiomyocytes by carvedilol.

Bach2 expression was detected by QRT-PCR in left ventricles from adult mice stimulated with carvedilol (Carv: 19 mg/kg per day) or vehicle for 3 day (A) or 7 days (B). N = 4–6. Data are shown as fold induction of Bach2 expression normalized to Gapdh. Unpaired 2-tailed t-test. *P < 0.05 or **P < 0.01 vs. DMSO. NS: not significant. C–F Primary adult human CFs (HCFs) as well as AC-16, H9c2, and HL-1 cardiomyocytes were treated with 1 μM Carv for 4 or 24 h (H) and subjected to either normoxia (basal) or hypoxia/reoxygenation (H/R). QRT-PCR analyses for the expression of BACH2 genes were then performed. Carv activates the expression of BACH2 genes in HCFs (C), AC-16 cells (D), H9c2 cells (E), and HL-1 cells (F) subjected to H/R. Moreover, the expression of BACH2 genes is downregulated in HCFs as well as AC-16, H9c2, and HL-1 cardiomyocytes after H/R. Data are shown as the fold induction of expression normalized to GAPDH genes. N = 4–6 per group. Two-way ANOVA with Tukey’s multiple comparison test. *P < 0.05 or **P < 0.01 vs. DMSO. #P < 0.05, ##P < 0.01, or ###P < 0.001 vs. normoxia. Data are presented as the mean ± SEM.

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