The cause of preeclampsia is unknown but it is linked to a variety of risk factors – antipohospholipid syndrome (APS) (an autoimmune disease) where the antibodies react to proteins present on the surface of cells.
Studies were conducted to see how APS causes preeclampsia where the pregnant mice were injected with APS antibodies and the animal developed high blood pressure and the amount of protein in urine also increased (characteristics of preeclampsia). In contrast the APS antibodies did not have any effect on non-pregnant mice.
Previous studies have shown that a protein called ApoER2 may be related to harmful actions of APS antibodies on placental cells. These cells normally pass from the fetal side of the placenta to the maternal side placenta to provide nutrition and it does not make the connection in preeclampsia.
In the mice the APS antibodies prevented the trophoblast migration and the growth of the fetus was restricted and in the mice without ApoER2 in trophoblast, the fetus developed normally despite APS antibody treatment.
Then scientists found that in the presence of APS antibodies the ApoER2 triggers the activity of PP2A (an enzyme that regulates protein function). Further studies have shown that in pregnant mice with APS antibodies, the PP2A increased trophoblast production of proteins that are involved in preeclampsia.
Scientists gave pregnant mice a drug to inhibit PP2A and they were protected from preeclampsia and the treatment had no side effects.
According to Dr.Shaul Hoping to translate these findings to human patients, the scientists examined placentas from women with APS, finding that they too had increased activity of PP2A. However, in a surprising turn, they discovered that compared with placentas from normal pregnancies, those from preeclamptic patients without APS also had increased PP2A activity, suggesting that this mechanism could be operating in a variety of forms of preeclampsia.
Further research is needed to give proper treatment for preeclampsia and stop premature delivery.
Source: Medindia
