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Abnormal placental development and early embryonic lethality in EpCAM-null mice
Keisuke Nagao1, Jianjian Zhu, Mallorie B Heneghan
1Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Plos One
|January 5, 2010
Summary
EpCAM is crucial for embryonic development, particularly placental function and maternal-fetal circulation. EpCAM deficiency in mice leads to in utero death by E12.5 due to severe placental abnormalities.
Area of Science:
- Developmental Biology
- Molecular Biology
- Immunology
Background:
- Epithelial cell adhesion molecule (EpCAM) is encoded by the tacstd1 gene.
- EpCAM is expressed in various normal and malignant epithelial cells and leukocytes.
- Previous in vitro studies suggested EpCAM functions as an intercellular adhesion molecule, with recent research linking it to cancer stem cells.
Purpose of the Study:
- To investigate the in vivo function of EpCAM.
- To characterize the developmental role of EpCAM using a knockout mouse model.
Main Methods:
- Generation of EpCAM knockout (EpCAM -/-) mice by disrupting the tacstd1 allele.
- Utilized gene trapping to create a fusion protein of EpCAM's N-terminus and betageo.
- Examined EpCAM expression patterns and developmental phenotypes in EpCAM +/- and EpCAM -/- embryos.
Main Results:
- EpCAM +/- mice were viable and fertile with no apparent abnormalities.
- EpCAM -/- mice exhibited embryonic lethality by E12.5, showing developmental delays and severe placental defects.
- Placentas of EpCAM -/- embryos had reduced vascularity, thin labyrinthine layers, and a dramatic decrease in parietal trophoblast giant cells.
Conclusions:
- EpCAM is essential for parietal trophoblast giant cell differentiation and survival.
- Normal development of the placental labyrinth and maternal-fetal circulation requires EpCAM.
- EpCAM plays a role in the development of vital organs, including the gut, kidneys, pancreas, lungs, eyes, and limbs.
