Manuscript:

Causative Effects of Genetically Determined High Maternal/Fetal Endothelin-1 on Preeclampsia-Like Conditions in Mice

 

 

Why I selected this manuscript?

It describes a study in mice with a modified Edn1 allele that increases mRNA stability and thereby elevates ET-1 levels. By making use of heterozygous pregnant females, as well as wildtype females mated with heterozygous males, the authors are capable of distinguishing in a very elegant way the contribution of maternal ET-1 and fetal ET-1 in pregnancy. It turns out that high maternal ET-1 production causes a preeclampsia-like phenotype, while fetal ET-1 increases the levels of the VEGF-inactivating factor sFlt-1, thus additionally contributing to blood pressure elevation. In a previous study in pregnant women with and without preeclampsia (Verdonk et al., Hypertension 2015), we observed a close relationship between ET-1, blood pressure and sFlt-1, and the current study now unravels the underlying cause of this relationship. Both studies suggest that ET receptor antagonists might be a promising tool to treat preeclampsia.