Funding outcome

Five to 7% of pregnant women develop preeclampsia (PE). These mothers have high blood pressure, inflammation and poor organ function. Severe cases of PE lead to more than 76,000 maternal and 500,000 infant deaths worldwide. As well, this can lead to sick newborns especially if they are premature. There are also longterm effects on the health of both the mother and her child as the age. The cause of PE remains unknown; however the placenta plays a major role in this disorder. One specific inflammatory molecule that is increased in ' the placentas and blood of mothers with PE is called tumour necrosis factor alpha (TNF-a). High levels of TNF-a can cause cell death in the placenta and reduce the delivery of nutrients and oxygen to the fetus. However, normal levels of TNF-a are needed for normal development of the fetus. So blocking all the effects of TNF-a to protect against PE is not a good treatment. However, if we can determine that the damaging effect of TNF-a occurs by increasing another factor, we could then block that factor while leaving the beneficial function of TNF-a alone. This other factor may be a lipid called sphingosine 1-phosphate (S1P) which is also increased In PE. S1P controls cell responses by binding to several specific receptors found on cells. One receptor called S1PR2 is increased on placentas from women with PE and S1P binding to S1PR2 may cause cell death in the placenta. However, TNF-a and S1 P levels have not yet been measured together in the blood of mothers with PE. We plan to do this to see if they are both increased compared to mothers with normal pregnancies. We will also measure the amounts of S1PR2 in placentas from women with PE and normal pregnancies. We predict that both TNF-a and S1P will be increased in the blood of mothers with PE and that S1PR2 amounts will also be increased in placentas from those same mothers. This study will help us to better understand how placental damage takes place and to create new treatments for pregnant mothers with PE.