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Rat liver epidermal growth factor receptors in intrauterine growth retarded and heavy-for-date fetuses
K Shigeta1, Y Hiramatsu, K Eguchi
1Department of Obstetrics and Gynecology, Okayama University Medical School, Japan.
Insights
Intrauterine growth retardation (IUGR) and heavy-for-dates (HFD) fetal rats show altered epidermal growth factor (EGF) receptor binding. IUGR rats upregulate EGF receptors, while HFD rats exhibit increased EGF consumption and lower urinary EGF excretion.
Area of Science:
- Developmental Biology
- Endocrinology
- Perinatal Medicine
Background:
- Epidermal Growth Factor (EGF) plays a crucial role in fetal development.
- Previous studies indicated lower urinary EGF levels in intrauterine growth retardation (IUGR) and heavy-for-dates (HFD) infants.
- Mechanisms controlling EGF levels during fetal growth require further investigation.
Purpose of the Study:
- To investigate the role of EGF receptors in regulating EGF levels during fetal growth.
- To compare EGF receptor binding in fetal rats with IUGR, HFD, and control phenotypes.
Main Methods:
- Fetal rats were categorized into IUGR, control, and HFD groups.
- EGF receptor binding assays were performed on fetal rat liver tissue.
- Statistical analysis (p < 0.05) was used to compare binding between groups.
Main Results:
- EGF binding to fetal rat liver increased significantly between days 19-21 of gestation.
- IUGR (380 +/- 57 fmol/mg protein) and HFD (545 +/- 112 fmol/mg protein) groups showed significantly greater EGF binding compared to controls (258 +/- 47 fmol/mg protein).
- IUGR rats demonstrated increased EGF receptor expression, suggesting a compensatory mechanism for low EGF.
Conclusions:
- IUGR in rats may be associated with compensatory upregulation of EGF receptors.
- HFD rats appear to consume more EGF, leading to decreased urinary EGF excretion.
- EGF signaling and receptor dynamics are closely linked to fetal growth regulation.
Abstract:
We recently reported that epidermal growth factor (EGF) levels in the first urine to be voided by intrauterine growth retardation (IUGR) and heavy-for-dates (HFD) infants were lower than control infants (8). In this study, we analyzed EGF receptors to reveal the mechanisms controlling EGF levels. EGF binding to fetal rat liver increased markedly from day 19-21 of gestation. Fetal rats were divided into IUGR, control and HFD groups. EGF binding to the liver in each group was as follows, IUGR; 380 +/- 57 fmol/mg protein, control; 258 +/- 47, and HFD; 545 +/- 112. The binding to IUGR and HFD rat liver was significantly greater than in the control group (p < 0.05). These data suggest that IUGR rats compensate for a lack of EGF by increased receptor expression and that HFD rats consume more EGF and have decreased urinary EGF excretion. These data also suggest that EGF is closely related to fetal growth and may play some important roles in fetal growth.