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Pregnancy-associated diamine oxidase originates from extravillous trophoblasts and is decreased in early-onset preeclampsia.

TitlePregnancy-associated diamine oxidase originates from extravillous trophoblasts and is decreased in early-onset preeclampsia.
Publication TypeJournal Article
Year of Publication2018
AuthorsVelicky, P, Windsperger, K, Petroczi, K, Pils, S, Reiter, B, Weiss, T, Vondra, S, Ristl, R, Dekan, S, Fiala, C, Cantonwine, D, McElrath, T, Jilma, B, Knöfler, M, Boehm, T, Pollheimer, J
JournalSci Rep
Volume8
Issue1
Pagination6342
Date Published2018 Apr 20
ISSN2045-2322
KeywordsCOLAB, Global Pregnancy Collaboration (CoLab)
Abstract

Human extravillous trophoblast (EVT) invasion of the pregnant uterus constitutes a pivotal event for the establishment of the maternal-fetal interface. Compromised EVT function manifesting in inadequate arterial remodeling is associated with the severe pregnancy disorder early-onset preeclampsia (eoPE). Recent studies suggest that EVTs invade the entire uterine vasculature including arteries, veins and lymphatics in the first trimester of pregnancy. We therefore hypothesized that EVT-derived factors accumulate in the circulation of pregnant women early in gestation and may serve to predict eoPE. In contrast to published literature, we demonstrate that placenta-associated diamine oxidase (DAO) is not expressed by maternal decidual cells but solely by EVTs, especially when in close proximity to decidual vessels. Cultures of primary EVTs express and secret large amounts of bioactive DAO. ELISA measurements indicate a pregnancy-specific rise in maternal DAO plasma levels around gestational week (GW) 7 coinciding with vascular invasion of EVTs. Strikingly, DAO levels from eoPE cases were significantly lower (40%) compared to controls in the first trimester of pregnancy but revealed no difference at mid gestation. Furthermore, DAO-containing pregnancy plasma rapidly inactivates pathophysiologically relevant histamine levels. This study represents the first proof of concept suggesting EVT-specific signatures as diagnostic targets for the prediction of eoPE.

DOI10.1038/s41598-018-24652-0
Alternate JournalSci Rep
Citation Key558
PubMed ID29679053
PubMed Central IDPMC5910386
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