Please use this identifier to cite or link to this item: https://doi.org/10.1126/science.aam6607
Title: ELABELA Deficiency Promotes Preeclampsia and Cardiovascular Malformations in Mice
Authors: LENA HO WAI MUN 
MARIE VAN DIJK
SAM TAN JIAN CHYE
DANIEL M MESSERSCHIMDT
SERENE CHNG
SHEENA ONG
LING KA YI
SOUAD BOUSSATA
GRACE GOH HUI YI
GJIS B AFINK
LIM CHIN YAN 
RAY DUNN
DAVOR SOLTER
BARBARA K KNOWLES
BRUNO REVERSADE 
Keywords: Peptides
Hormones
Pregnancy
Cardiovascular
Issue Date: 18-Aug-2017
Publisher: American Association for the Advancement of Science
Citation: LENA HO WAI MUN, MARIE VAN DIJK, SAM TAN JIAN CHYE, DANIEL M MESSERSCHIMDT, SERENE CHNG, SHEENA ONG, LING KA YI, SOUAD BOUSSATA, GRACE GOH HUI YI, GJIS B AFINK, LIM CHIN YAN, RAY DUNN, DAVOR SOLTER, BARBARA K KNOWLES, BRUNO REVERSADE (2017-08-18). ELABELA Deficiency Promotes Preeclampsia and Cardiovascular Malformations in Mice. Science 357 (6352) : 707-713. ScholarBank@NUS Repository. https://doi.org/10.1126/science.aam6607
Rights: Attribution-NonCommercial 4.0 International
Abstract: Preeclampsia (PE) is a gestational hypertensive syndrome affecting between 5 and 8% of all pregnancies. Although PE is the leading cause of fetal and maternal morbidity and mortality, its molecular etiology is still unclear. Here, we show that ELABELA (ELA), an endogenous ligand of the apelin receptor (APLNR, or APJ), is a circulating hormone secreted by the placenta. Elabela but not Apelin knockout pregnant mice exhibit PE-like symptoms, including proteinuria and elevated blood pressure due to defective placental angiogenesis. In mice, infusion of exogenous ELA normalizes hypertension, proteinuria, and birth weight. ELA, which is abundant in human placentas, increases the invasiveness of trophoblast-like cells, suggesting that it enhances placental development to prevent PE. The ELA-APLNR signaling axis may offer a new paradigm for the treatment of common pregnancy-related complications, including PE.
Source Title: Science
URI: https://scholarbank.nus.edu.sg/handle/10635/168375
ISSN: 10959203
00368075
DOI: 10.1126/science.aam6607
Rights: Attribution-NonCommercial 4.0 International
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