Decreased H3K9ac level of AT2R mediates the developmental origin of glomerulosclerosis induced by prenatal dexamethasone exposure in male offspring rats

The selection and identification of compound housekeeping genes for quantitative real‐time polymerase chain reaction analysis in rat fetal kidney

“…In order to further verify whether the double housekeeping genes can be more beneficial to obtain the accurate experimental conclusion, we conducted a verification test of the target gene in the PDE‐induced IUGR model. Our previous studies had confirmed that the mRNA expression of nephrin was significantly decreased in fetal offspring induced by PDE (Li et al, 2019). Nephrin is specifically expressed in kidney podocytes, and it has high expression abundance (Dlugos et al, 2019; Fukusumi et al, 2018); thus, we used it to carry out the verification experiments of compound housekeeping genes.…”

“…To verify the stability and accuracy of the screened housekeeping genes, we designed a target gene verification experiment. Nephrin , a podocyte marker gene, has been proved to be poorly expressed in fetal kidneys in the PDE‐induced IUGR model (Li et al, 2019; Zhu et al, 2019). In this study, we detected the expression of nephrin mRNA in the fetal kidney of male rats in the PDE‐induced IUGR model and conducted relatively quantitative analysis with single housekeeping gene and multiple housekeeping genes, respectively.…”

“…On the basis of the dose conversion between humans and rats (1:6.16) (Reagan‐Shaw et al, 2008), treatment with dexamethasone in rats at 0.2 mg/kg·day in this study is comparable with that used in humans at 0.03 mg/kg·day, while the standard dose of dexamethasone in clinical treatment during pregnancy is 0.05–0.2 mg/kg·day (Miracle et al, 2008). Therefore, based on the clinical treatment status and the characteristics of renal development, we subcutaneously administrated 0.2 mg/kg·day (0.1 ml/100 g) dexamethasone on gestational Days (GD) 9–20 to establish the PDE rat model (Li et al, 2019). The body weight of pregnant rats during the treatment period were about 280 ± 20 g–385 ± 30 g.…”

Maternally derived glucocorticoid inhibits adrenal development in offspring induced by prenatal dexamethasone exposure via IGF1

“…Numerous studies have suggested that glucocorticoid-induced intrauterine programming alterations are related to abnormal expression of some critical genes regulated by miRNAs (Clayton et al , 2018), and miRNAs can regulate histone acetylation and expression levels of downstream target genes by targeting histone deacetylase (Gao et al , 2018;Xing et al , 2019). Our recent studies have confirmed that abnormal histone acetylation modification was involved in multi-organ development programming and related disease susceptibility caused by PDE (Liu et al , 2018;Xiao et al , 2018;Li et al , 2019). Therefore, we speculate that low levels of maternally derived glucocorticoid caused by PDE may regulate IGF1 histone acetylation and expression through miRNAs in fetal adrenal, thereby resulting in its abnormal function development in offspring.…”

Selection and Validation of the Optimal Panel of Reference Genes for RT-qPCR Analysis in the Developing Rat Cartilage

“…Therefore, fetalmaternal glucocorticoid overexposure under prenatal adverse environmental exposure can be a common phenomenon. Moreover, the IUGR model induced by prenatal dexamethasone exposure (PDE) is a classic method (Tomaszewska et al, 2012;Conti et al, 2017;Chen et al, 2018;Liu et al, 2018;Xiao et al, 2018;Li et al, 2019;Wu et al, 2019). Dexamethasone, as a synthetic glucocorticoid, is easy to enter fetus through the placenta (Morales et al, 1986), so the IUGR model induced by PDE can well simulate the overexposure of glucocorticoid in prenatal adverse environments during the development of offspring rats.…”