LAUSR

Villie et al. ELABELA concentration in maternal plasma. Am J Obstet Gynecol 2019. OBJECTIVE: ELABELA (ELA), an endogenous ligand for the apelin receptor (APLR), is a peptidic hormone expressed both by the kidneys and placenta. Via the endothelial receptor APLR, secretion of ELA seems to be critical for mouse placental angiogenesis and endothelial tipping. In gravid mice carrying ELA-deficient embryos, placental insufficiency of vascular origin and hallmarks of preeclampsia [PE] are present. However, the level of current evidence linking the human maternal preeclamptic phenotype to maternal blood soluble form of VEGF-R1 (sflt1) increase is so high, and the hypoxic RNA signal in ELA-deficient placentas so strong, that the lack of sFlt1 increase, at the protein level, in the murine model is puzzling. Two human studies subsequently found no ELA decrease in maternal blood, either at delivery in women with preterm PE (mean gestational ages, 29.4 and 30.8 weeks), or in late-onset PE (mean gestational age, 37.6 weeks), whereas ELA was actually increased. Given these contradictory findings and the claim that ELA acts independently and earlier than sFlt1, we investigated whether ELA was dysregulated before PE onset.