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Preeclampsia is one of the most common causes of maternal and fetal morbidity and mortality worldwide. A protein called
placental protein 13 (here: eclampsin), only found to be produced in placenta, has been shown to precondition the uterine
arteries in the first trimester, preventing the woman to develop preeclampsia. Women having low eclampsin concentration
in first trimester will develop preeclampsia later in pregnancy. Being only 32kDa in size, this small protein may be delivered
as therapeutics, to those women in risk of developing preeclampsia.


Today, the only "cure" for women who develop preeclampsa is early delivery and removal of the placenta that is the source
for the disorder. The use of magnesium sulphate help to prevent the disease exacerbation to eclampsia but does not
prevent the women from experiencing the major damages of hypertension and kidney failure that takes months to recover.
None is capable of preventing the prematurity occur when the disease develop early.


In addition to being a world-wide problem and there is need for a drug or a method to cure this disease, since the only
cure today is delivery of the baby and removing the placenta from the mother. The impact of preeclampsia disappears
after delivery, but affected women are 5-13 times more vulnerable to develop cardiovascular diseases and diabetes, which
shorten their longevity by 5-10 years. Their offspring’s stressful "memory" is accompanied by an increased susceptibility to
obesity and diabetes already in adolescence. This "disease" has considerable impact on world health.


PP13-placental-liningBased on our research, we suggest that eclampsin (placental protein 13) is involved in generating a systemic endothelial effect within the mother, such as uterine vascular remodeling and peripheral vasodilatation. Women with low serum eclampsin levels in the first trimester of pregnancy lack the necessary amount of this factor to enable immune-tolerance and to prepare the systemic endothelium for the increased blood flow needed to supply the fetus with nutrients during the second half of pregnancy. If endothelial adaptation or pre-conditioning has not occurred in the first trimester, placental development might be impaired resulting in an increased release of placental factors that negatively affect the maternal endothelium in the second half of pregnancy. This will finally culminate in the clinical symptoms of preeclampsia including increased blood pressure and renal failure.

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