Written By: Longjam Dineshwori | Updated : September 15, 2021 11:12 AM IST
Image credits by: Preeclampsia can be deadly for gestating mothers and their babies.
Preeclampsia is a dangerous pregnancy complication characterized by the development of high blood pressure and excess protein in the urine. It is estimated to affect 5 to 7 per cent of pregnant women worldwide. Preeclampsia can be deadly for gestating mothers and their babies. Often premature delivery is the only option in preeclampsia, and we know that premature birth can be life-threatening for babies and lead to lifelong consequences.
While it's not clear what exactly causes preeclampsia, a variety of risk factors are linked to the condition. One is antiphospholipid syndrome (APS), an autoimmune disease in which antibodies react to proteins on the surface of some cells. APS is rare disease, affecting only about 5 in every 100,000 people. However, APS antibodies have been found in about 29 per cent of pregnant women with preeclampsia.
A team of UT Southwestern scientists conducted a study to better understand how APS leads to preeclampsia, and found an enzyme called protein phosphatase 2 (PP2A) that appears to be a major driver of preeclampsia. They published the findings in Circulation Research, suggesting that it could lead to new treatments for preeclampsia that are far better for both mothers and babies, other than premature delivery.
The UT Southwestern scientists led by Dr. Philip W. Shaul, Professor and Vice Chair for Research in the Department of Pediatrics injected with APS antibodies in pregnant and non-pregnant mice. The pregnant animals developed high blood pressure and a rise in urine protein (which are characteristics of preeclampsia), but the blood pressure in nonpregnant mice remained unaffected.
Previous work had suggested that a protein called ApoER2 may be related to the harmful actions of APS antibodies on placental cells called trophoblasts, which normally travel from the fetal side of the placenta to the maternal side to provide the fetus with nutrients. In preeclampsia, these cells don't successfully make that connection.
In mice model, the researchers found that the APS antibodies prevented trophoblast migration, and thus the growth of the fetus was restricted. But in genetically engineered mice without ApoER2 in trophoblasts, the presence of APS antibodies didn't affect the development of the fetuses, and the mothers also didn't develop preeclampsia.
But ApoER2 protein is not the only culprit. ApoER2 triggers the activity of PP2A, an enzyme that regulates protein functions throughout the body, in the presence of the APS antibodies. Heightened activity in PP2A then increased trophoblast production of proteins associated with preeclampsia, the researchers said.
The researcher found that when the pregnant mice were treated with a drug that inhibits PP2A, they were protected from preeclampsia, without any apparent harmful effects on the mothers or their gestating babies.
Increased activity of PP2A was also seen in placentas from women with APS. But the researchers were surprised to find that those placentas from preeclamptic patients without APS also had increased PP2A activity, indicating that this mechanism could be operating in different forms of preeclampsia.
Based on these findings, Dr. Shaul believe that treatments targeting PP2A or its related machinery in the trophoblast may be a better way to tackle preeclampsia in pregnant women.
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