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Effect of ethanol on the development of visceral yolk sac
1Department of Nutrition & Food Hygiene, Laboratory of Molecular Toxicology & Developmental Molecular Biology, School of Public Health, Peking University, Beijing, China.
Insights
Prenatal ethanol exposure harms mouse embryo development by damaging the visceral yolk sac (VYS). This damage, including suppressed gene expression, likely contributes to birth defects and fetal alcohol syndrome.
Area of Science:
- Developmental biology
- Toxicology
- Teratology
Background:
- Prenatal ethanol exposure causes developmental retardation and malformations.
- The visceral yolk sac (VYS) is crucial for nutrient transport before placental formation.
- Yolk sac dysfunction is linked to mammalian embryonic malformations.
Purpose of the Study:
- To investigate the impact of ethanol on visceral yolk sac (VYS) development in mouse embryos.
- To assess the effects of ethanol on VYS structure, function, and gene expression.
Main Methods:
- In vitro culture of 8.5-day mouse embryos exposed to varying ethanol doses.
- Microscopic examination (light and electron) of VYS development.
- Analysis of vasculogenesis-related gene expression (Flk1, Tie2) via RT-PCR.
Main Results:
- Ethanol exhibited dose-dependent toxicity to the VYS, reducing diameter and protein/DNA content.
- Suppressed VYS development, including vitelline vessels, correlated with embryo malformations.
- Ethanol repressed key vasculogenesis genes (Flk1, Tie2) and altered VYS endodermal cell histology/function.
Conclusions:
- Impaired VYS development is a potential mechanism for ethanol-induced teratogenicity in mice.
- Findings offer insights into human fetal alcohol syndrome pathogenesis.
Background:
Prenatal ethanol exposure can cause development retardation and malformations in human offspring. Before the formation of chorioallantoic placenta, yolk sac plays an important role in transporting nutrients from the mother to the embryo. Functional suppression of yolk sac is found to be relevant to the malformations in mammalian embryos.
Methods:
Female 8.5-day C57BL/6J mouse embryos were cultured in vitro and exposed to different doses of ethanol. The development of visceral yolk sac (VYS) was examined with light and electron microscopes. The expression profiles of some vasculogenesis-related genes were detected with reverse transcription-PCR.
Results:
A dose-dependent toxicity to the VYS was found, including reduced diameter, decreased protein and DNA contents, and suppressed development of vitelline vessels. The hypogenesis of VYS agreed with the retarded development and/or malformations found in the embryos. Histological and functional alterations were found in the ethanol-exposed VYS endodermal cells. The expressions of vasculogenesis-related genes, fetal liver kinase 1 (Flk1) and tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (Tie2), were repressed by ethanol.
Conclusions:
Impaired structural and functional development of VYS may contribute to the teratogenic action of ethanol in mice, which may also provide a clue to the study of fetal alcohol syndrome in humans.
