Preeclampsia is a regrettably common cause of premature birth, which can be life-threatening for babies and lead to lifelong consequences. Through identifying PP2A's role in this condition, we may be able to develop treatments for preeclampsia that are far better for both mothers and babies," said study leader Philip W. Shaul, M.D., Professor and Vice Chair for Research in the Department of Pediatrics at UTSW and Director of the Center for Pulmonary and Vascular Biology. Dr. Shaul co-led this study with Chieko Mineo, Ph.D., Professor of Pediatrics and Cell Biology.

Based on previous work, the researchers knew that a protein called ApoER2 may be related to the harmful actions of APS antibodies on placental cells called trophoblasts. These cells, which normally journey from the fetal side of the placenta to the maternal side to provide the fetus with nutrients, don't successfully make that connection in preeclampsia. In mice, the APS antibodies prevented trophoblast migration, and growth of the foetus was restricted. When the researchers genetically engineered mice without ApoER2 in trophoblasts, the fetuses developed normally despite APS antibody treatment, and the mothers were protected from developing preeclampsia.

But the scientists knew that ApoER2 didn't tell the whole story. They found that in the presence of the APS antibodies, ApoER2 triggers the activity of PP2A, an enzyme that regulates protein functions throughout the body. Further experiments showed that in the pregnant mice with APS antibodies, heightened activity in PP2A increased trophoblast production of proteins known to be involved in preeclampsia.

Regards

John
EditorialAssistant
Immunogenetics Open Access