Fig. 6: Effects of dexamethasone on osteogenic differentiation and renin–angiotensin system in bone marrow mesenchymal stem cells (BMSCs). | Cell Death & Disease

Fig. 6: Effects of dexamethasone on osteogenic differentiation and renin–angiotensin system 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. 6

a RT-qPCR analysis of gene expression of Runx2, alkaline phosphatase (ALP), bone sialoprotein (BSP), osteocalcin (OCN) in BMSCs cultured in the osteogenic medium and treated with different concentrations of dexamethasone for 14 days. b RT-qPCR analysis of gene expression of adipogenic differentiation markers, including peroxisome proliferator-activated receptor gamma (PPARγ) and fatty acid-binding protein 4 (FABP4) in BMSCs. c 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 BMSCs cultured in the osteogenic medium and treated with different concentrations of dexamethasone for 14 days. d Western blotting assay of ACE, AT1R, and AT2R protein level in BMSCs. e Alizarin Red S staining for mineralization nodules after co-treating BMSCs with dexamethasone and ACE inhibitor (ACEI) during the process of osteogenic differentiation. f RT-qPCR analysis of gene expression of Runx2, ALP, BSP, and OCN after co-treating BMSCs with dexamethasone and ACEI. g RT-qPCR analysis of gene expression of PPARγ and FABP4 after co-treating BMSCs with dexamethasone and ACEI. 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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