Messenger substance of the immune system apparently promotes the development of preeclampsia
But why do the bodies of women with preeclampsia produce more CYP2J2 and thus more EET? Tumor necrosis factor-alpha (TNF-alpha), a chemical messenger of the immune system, could possibly contribute. This signaling substance is released at early stages of pregnancy whenever placental blood flow is too low, causing oxygen deficiency. As the researchers showed, TNF-alpha promotes the production of CYP2J2 and EET in the placenta. In other tissues, this reaction would be useful, since EET rescues tissue from dying that has an insufficient supply of blood and therefore of oxygen. In the placenta, by contrast, this boost in production of CYP2J2 and EET could lead to a vicious circle. The trophoblasts do not grow as well into the decidua and the blood vessels and are not remodeled correctly, so that blood flow through the placenta and blood supply to the fetus deteriorates. As a consequence, the mothers becomes hypertensive and EETs under these conditions is converted in such a way that the blood pressure continues to increase.
Treatment of preeclampsia, which according to estimates costs many thousands of maternal lives across the globe every year, remains difficult. The only possibility is to induce delivery at an early stage if the clinical presentation is severe. In Germany, preeclampsia is the cause for up to 20,000 premature births annually. Once the child is born, the symptoms subside in the mother. Nevertheless, she may suffer long-term increased risk for cardiovascular disease and develop heart attack, stroke, or hypertension at an early age. For the child, depending on the stage of fetal development, the premature birth may result in death or severe lifelong disability, and the child may also have an increased risk for cardiovascular disease later on. The research conducted by Dr. Herse, the entire team, and Dr. Dech
|Contact: Barbara Bachtler|
Helmholtz Association of German Research Centres