2018 Volume 9 Issue 2 Pages 63-71
The hypothesis of the “development origins of health and diseases” addresses the risk of chronic kidney disease in adulthood. This study aimed to investigate whether prenatal glucocorticoid (GC) administration is associated with fetal kidney maturation. We investigated the effects of prenatal GC administration on the expression of the prorenin receptor (PRR) and extracellular signal-regulated kinase (ERK) required for development in the fetal rat.
Dexamethasone (DEX) was administered to pregnant rats for 2 days on days 17 and 18 or days 19 and 20 of gestation, and the kidney tissues of 19- and 21-day fetuses and 1-day-old neonates were analyzed by immunohistochemistry. The viability of human embryonic kidney (HEK)293 cells exposed to DEX for 24 h was determined by MTT assay, and mRNA and protein expressions of the PRR, ERK, and phospho(p)-ERK were analyzed using real-time PCR and Western blotting.
ERK-positive areas were observed in primitive perivascular mesenchymal cells and immature glomeruli of the fetal rats. ERK-positive areas were significantly increased in the kidneys of 21-day fetuses compared with those of 19-day fetuses. DEX tended to increase ERK- and p-ERK-positive areas in the kidney of 19-day fetuses, and their levels tended to reach the expression levels of 21-day fetuses. Although the number of PPR-positive areas did not change with DEX administration, they were localized in ureteric bud branches and collecting ducts. DEX also significantly increased the mRNA and protein levels of ERK, p-ERK, and PRR in HEK293 cells.
Taken together, these results indicate that prenatal DEX administration may contribute to kidney development through an increase in ERK in the immature fetal rat.
