Fig. 4: Effects of prenatal dexamethasone exposure (PDE) on the histone acetylation level of angiotensin-converting enzyme (ACE) and its intrauterine programming mechanism in F1 male offspring. | Cell Death & Disease

Fig. 4: Effects of prenatal dexamethasone exposure (PDE) on the histone acetylation level of angiotensin-converting enzyme (ACE) and its intrauterine programming mechanism in F1 male offspring.

From: Increased H3K27ac level of ACE mediates the intergenerational effect of low peak bone mass induced by prenatal dexamethasone exposure in male offspring rats

Fig. 4

a ChIP assay of the histone 3 lysine 9 acetylation (H3K9ac) and H3K27ac level in ACE promoter region on gestational day (GD) 20. b ChIP assay of the H3K9ac and H3K27ac level in ACE promoter region at postnatal week (PW) 2. c ChIP assay of the H3K9ac and H3K27ac level in ACE promoter region at PW12. d RT-qPCR analysis of glucocorticoid receptor (GR) expression in fetal bone tissue from the control and PDE groups. e RT-qPCR analysis of gene expression of transcription factors related to the function of GR, including nuclear transcription factor-κB (NF-κB), CCAAT/enhancer-binding protein α (C/EBPα), c-Fos, c-Jun, special protein 1 (SP1) in fetal bone tissue from the control and PDE groups. f RT-qPCR analysis of gene expression of p300 in fetal bone tissue from the control and PDE groups. Mean ± S.E.M., n = 8 per group, *P < 0.05, **P < 0.01 compared with the control

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