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Published on: November 20, 2015
Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes
Tsukasa Kobayashi1, Yuko Takeba2, Yuki Ohta1
1Department of Pharmacology, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki, Kanagawa, 216-8511, Japan.
Insights
Prenatal glucocorticoid (GC) administration promotes preterm rat hepatocyte maturation. This treatment increased hepatocyte size and key maturation markers, suggesting a beneficial effect on immature livers.
Area of Science:
- Developmental Biology
- Neonatal Medicine
- Hepatology
Background:
- Prenatal glucocorticoid (GC) administration is used to mature fetal cardiopulmonary systems in cases of preterm birth risk.
- Immature livers in preterm infants can lead to postnatal dysfunction.
- The impact of prenatal GC exposure on liver maturation is not fully understood.
Purpose of the Study:
- To investigate the effects of prenatal glucocorticoid administration on the maturation of liver hepatocytes in preterm rat models.
Main Methods:
- Pregnant Wistar rats received Dexamethasone (DEX) on specific gestational days before cesarean section.
- Real-time RT-PCR, immunohistochemical staining, and ELISA were used to analyze liver samples.
- Key markers including albumin, HNF4α, HGF, Thy-1, cyclin B, and CDK1 were quantified.
Main Results:
- Prenatal DEX administration resulted in enlarged hepatocytes, indicating enhanced growth.
- Levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), and hepatocyte growth factor (HGF) were elevated.
- Cell cycle markers cyclin B and CDK1 showed decreased levels, suggesting cell cycle exit and maturation.
Conclusions:
- Prenatal glucocorticoid administration promotes hepatocyte maturation in preterm fetuses.
- This maturation is associated with the upregulation of HNF4α and HGF expression.
Background:
Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration on the maturation of liver hepatocytes in preterm rats.
Methods And Results:
Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), hepatocyte growth factor (HGF), thymus cell antigen 1 (Thy-1), cyclin B, and Cyclin-dependent kinase 1 (CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production. The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.
Conclusions:
The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in preterm fetuses.
