Fig. 7: The molecular mechanism of the activated renin–angiotensin system (RAS) induced by dexamethasone in bone marrow mesenchymal stem cells (BMSCs). | Cell Death & Disease

Fig. 7: The molecular mechanism of the activated renin–angiotensin system (RAS) induced by dexamethasone in bone marrow mesenchymal stem cells (BMSCs).

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. 7

a Western blotting assay of glucocorticoid receptor (GR) protein level in cytoplasm and nucleus after treating BMSCs with dexamethasone. b ChIP assay of the histone 3 lysine 27 acetylation (H3K27ac) level in angiotensin-converting enzyme (ACE) promoter region in BMSCs treated with dexamethasone or co-treated with dexamethasone and GR inhibitor RU486. c Western blotting assay of CCAAT/enhancer-binding protein α (C/EBPα) and p300 protein level in nucleus after treating BMSCs with dexamethasone or co-treating BMSCs with dexamethasone and RU486. d ChIP assay of the H3K27ac level in ACE promoter region after co-treating BMSCs with dexamethasone and C/EBPα siRNA or p300 inhibitor C646. All experiments were performed at least three times. Mean ± S.E.M., *P < 0.05, **P < 0.01 compared with the untreated cells

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