A recent study by scientists from the UT Southwestern suggests that the appearance of an enzyme known as Protein Phosphatase 2 or PP2A is the major driver behind preeclampsia, a pregnancy complication where high blood pressure and excess protein in the mother's urine develop. Researchers hope that the study would aid in establishing new treatments for preeclampsia patients other than simulated premature delivery, which is often the sole option to save both the mother and the pregnancy.
What is Preeclampsia?
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According to the Mayo Clinic, pre-eclampsia is a complication during pregnancy where high blood pressure and signs of organ system damage, often the kidneys and liver, are observed on the mother. This usually begins after 20 weeks of pregnancy in women who otherwise had normal blood pressure up to this point.
If left untreated, this can lead to detrimental and even fatal complications for both the mother and the baby. If diagnosed with preeclampsia, the safest and most effective treatment today is to deliver the baby prematurely. Although, even after delivery, it takes some mothers a while to fully recuperate.
At times, preeclampsia may develop without noticeable symptoms. High blood pressure often develops slowly, which is why careful monitoring of a mother's blood pressure is a vital part of prenatal care. Other symptoms of preeclampsia include excess protein in the mother's urine, severe headaches, changes in vision, abdominal pain, nausea, and impaired liver function.
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How PP2A is a Major Driver Behind Preeclampsia?
Preeclampsia affects 5-7% of pregnancies worldwide and can be detrimental to the gestation of the mother and baby. Despite the causes behind preeclampsia remains a mystery, Dr. Shaul, co-author of a study published in the journal Circulation Research, titled "Protein Phosphatase 2A Activation via ApoER2 in Trophoblasts Drives Preeclampsia in a Mouse Model of the Antiphospholipid Syndrome," researchers have associated the adverse condition with a variety of risk factors. One known risk is an autoimmune disease and antiphospholipid syndrome, where antibodies react to the proteins found on the surfaces of vital cells.
The better understand the relationship between APS and preeclampsia, researchers created animal models by injecting pregnant lab mice with APS antibodies. These tests showed the mice developing high blood pressure, and a significant rise in urine protein with are characteristics of preeclampsia. However, the APS antibodies had no effect on the blood pressures of nonpregnant mice.
Based on previous research, a protein known as ApoER2 could be related to the harmful effects of APS antibodies on cells known as trophoblasts--placental cells. These cells that, under normal conditions, would journey from the fetal side to the maternal side of the placenta to provide nutrients aren't able to successfully make the connection in mice that have developed preeclampsia.
When researchers dosed the pregnant mice with PP2A drug inhibitors, they were safeguarded from preeclampsia needing no harmful treatment, nor did they develop adverse side effects that would affect the baby's gestation. Researchers also found that human pregnant women also had increased activity of PP2A reports NewsMedical.
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