Fig. 5: Effects of prenatal dexamethasone exposure (PDE) on the peak bone mass in F2 male offspring and its intergenerational mechanisms. | Cell Death & Disease

Fig. 5: Effects of prenatal dexamethasone exposure (PDE) on the peak bone mass in F2 male offspring and its intergenerational mechanisms.

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. 5

a Representative micro-CT images of femur from F2 male offspring at postnatal week (PW) 12. b Quantitative micro-CT analysis of trabecular bone microarchitecture. c RT-qPCR analysis of gene expression of Runx2, bone sialoprotein (BSP), alkaline phosphatase (ALP), osteocalcin (OCN) from F2 male offspring at PW12. d RT-qPCR analysis of gene expression of renin–angiotensin system (RAS), including angiotensin-converting enzyme (ACE), angiotensin receptors (ATRs) and ELISA analysis of angiotensin II (Ang II) production in bone tissue from F2 male offspring at PW12. e ChIP assay of the histone 3 lysine 9 acetylation (H3K9ac) and H3K27ac level in ACE promoter region from F2 male offspring at PW12. Scale bar = 500 μm. Mean ± S.E.M., n = 8 per group, *P < 0.05, **P < 0.01 compared with the control

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