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DNA methylation changed by 5-azacytidine can affect normal fetal and placental development

DNA methylation as a regulatory mechanism for mammalian gene expression is present in the process of placentation, as well as of fetal development. It can be changed by the demethylating agent 5-azacytidine, which gets incorporated into DNA instead of cytosine, prevents DNA methylation and subsequently changes expression of genes. By intraperitoneally applying 5-azaC to gravid female, we could investigate its effect on fetal nad placental development. The importance of DNA methylation status is documented very early on in embryonal development, already in the cleavage stage, where two distinct types of tissue are formed: embryoblast and trophoblast. They are the first differentiation in a young embryo, which is connected with a degree of DNA methylation. Present there is also gene Oct-4 as a marker of embryoblast tissue. Its expression is epigenetically regulated, i.e. it is hypermethylatied and deacetylated, and therefore inactive in trophoblast, as opposed to the hypomethylated and acetylated one, which is present in the future embryoblast. In this Commentary we will discuss our results obtained in exploring the influence of DNA demethylating agent 5-azaC on fetal and placental development as well as try to explain why this kind of investigation is important for understanding analoguos processes in humans.

5-azacytidine, epigenetic, DNA methylation, placenta, fetus

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