A groundbreaking study conducted by the German Cancer Research Center (DKFZ) and the Mannheim Medical Faculty of Heidelberg University has uncovered a critical epigenetic mechanism that controls the development of blood vessels in the placenta, a key factor for healthy fetal growth. The findings reveal that a specific enzyme involved in modifying gene activity plays a crucial role in the formation of these blood vessels, and its deficiency may be linked to pregnancy complications such as preeclampsia.
The placenta, a temporary organ during pregnancy, serves as a lifeline between the mother and fetus, providing essential nutrients and oxygen while removing waste. If blood vessels in the placenta fail to develop properly, it can lead to placental insufficiency, which disrupts the exchange of nutrients and oxygen, putting the fetus at risk. One of the most severe outcomes of this condition is fetal growth retardation.
Dr. Hellmut Augustin, vascular specialist at DKFZ and Heidelberg University, emphasized the importance of blood vessel formation in pregnancy, stating, “Abnormal growth of the placental blood vessels is the main cause of fetal growth retardation.” To better understand how such malformations occur, his team examined the blood vessels of the mouse placenta at a cellular level.
The research focused on the endothelial cells that line the blood vessels and play a vital role in forming new vessels. These cells, located in the mouse placenta’s area corresponding to the chorionic villi in humans, showed that gene activity in the endothelial cells decreases as they move from the maternal side to the fetal side of the placenta. This zonation is closely linked to the blood flow strength in the area.
Epigenetic mechanisms, particularly DNA methylation, regulate these changes in gene activity. By analyzing the DNA methylation enzymes, known as DNA methyltransferases, the researchers found that DNMT3A, a specific methyltransferase enzyme, was primarily responsible for methylating the fetal placental endothelium.
When DNMT3A was switched off in the endothelial cells of mice, the DNA methylation process was disrupted. This led to a loss of the spatial zonation in gene expression, impairing placental vascular development. As a result, the mice experienced growth retardation, an effect that persisted even after birth.
The team then cross-referenced these findings with gene data from pregnant women, comparing healthy placental endothelial cells to those from women suffering from preeclampsia, a condition that hampers placental blood supply and often results in growth restrictions. The results showed a similar reduction in DNMT3A expression in the placental endothelium of preeclampsia patients, supporting the mouse study’s findings.
This research suggests that DNMT3A plays a pivotal role in the healthy development of placental blood vessels. A deficiency in this enzyme could be a significant factor in the development of placental insufficiency and related complications like fetal growth retardation and preeclampsia. Understanding these mechanisms could lead to more targeted treatments for pregnancy disorders and improve outcomes for mothers and their babies.
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