New research from the German Cancer Research Center (DKFZ) reveals that the epigenetic enzyme DNMT3A plays a vital role in the proper development of blood vessels in the placenta. This discovery could have significant implications for understanding and treating pregnancy complications like preeclampsia.
In all female mammals, including humans, the developing fetus receives vital nutrients and oxygen through the placenta, a temporary organ connecting the fetus to the mother's bloodstream. Proper blood vessel development within the placenta is crucial for ensuring adequate nutrient and oxygen supply to the fetus. When this development is impaired, it can lead to placental insufficiency, a condition where the placenta doesn't deliver sufficient blood, jeopardizing fetal health.
This often results in fetal growth retardation, a serious concern for pregnancy outcomes.Scientists at the German Cancer Research Center (DKFZ) and the Mannheim Medical Faculty of Heidelberg University have made a significant discovery regarding the mechanisms behind placental blood vessel development. Their research, focusing on mouse models, revealed that epigenetic regulation plays a critical role in this process. Specifically, they identified a DNA methyltransferase enzyme, DNMT3A, as a key player in controlling gene activity within the endothelial cells that line the placental blood vessels. These cells are essential for forming new blood vessels and ensuring proper placental function.The researchers found that in a healthy placenta, the activity of certain genes in endothelial cells decreases from the maternal to the fetal side, a pattern linked to blood flow strength. This spatial zonation of gene expression is orchestrated by epigenetic modifications, such as DNA methylation, where DNMT3A primarily contributes to the methylation of the fetal placental endothelium. When DNMT3A was genetically deactivated in mouse models, DNA methylation decreased, disrupting the spatial zonation of gene expression and impairing placental vasculature development. This resulted in fetal growth retardation that persisted even after birth. Furthermore, the team analyzed gene databases and compared single-cell RNA sequence data from healthy placentas with those from women experiencing preeclampsia, a pregnancy complication known to cause fetal growth disorders due to placental insufficiency. They found a reduced expression of DNMT3A in the placental endothelium of preeclampsia patients, mirroring the findings in the mouse models. This correlation strengthens the evidence that DNMT3A plays a crucial role in healthy placental vessel development and that its deficiency could contribute significantly to placental insufficiency. This groundbreaking research sheds light on the intricate mechanisms underlying placental function and opens new avenues for understanding and potentially treating pregnancy disorders
Placenta Pregnancy Fetal Growth Epigenetics DNMT3A Preeclampsia
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