Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries. Brosens I, Brosens JJ, Muter J, Puttemans P, Benagiano G. Am J Obstet Gynecol 2019;221:219-26.

Gyselaers, Wilfried; Lees, C.; Valensise, H.; Thilaganathan, B.

doi:10.1016/j.ajog.2019.12.274

Cited by 5 publications

(2 citation statements)

References 4 publications

(3 reference statements)

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“…Doppler sonography is a useful method to assess uterine and umbilical artery flow impedance. Increased uterine artery Doppler pulsatility index and resistivity index have long been considered a result of abnormal spiral artery adaptation at implantation, but, currently, increasing number of experimental, clinical, and epidemiological data are in favor of the opposite pathway, suggesting abnormal placentation merely as the result rather than the cause of abnormal uterine perfusion ( 105 , 106 ). In this context, the inverse correlation between preconceptional uterine artery Doppler impedance measurements and subsequent birthweight in formerly preeclamptic women is illustrative ( 107 ).…”

Section: Interactive Maternal-fetal Hemodynamics In Fetal Growth Rest...mentioning

confidence: 99%

Maternal Low Volume Circulation Relates to Normotensive and Preeclamptic Fetal Growth Restriction

Gyselaers

Lees

2022

Front. Med.

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This narrative review summarizes current evidence on the association between maternal low volume circulation and poor fetal growth. Though much work has been devoted to the study of cardiac output and peripheral vascular resistance, a low intravascular volume may explain why high vascular resistance causes hypertension in women with preeclampsia (PE) that is associated with fetal growth restriction (FGR) and, at the same time, presents with normotension in FGR itself. Normotensive women with small for gestational age babies show normal gestational blood volume expansion superimposed upon a constitutionally low intravascular volume. Early onset preeclampsia (EPE; occurring before 32 weeks) is commonly associated with FGR, and poor plasma volume expandability may already be present before conception, thus preceding gestational volume expansion. Experimentally induced low plasma volume in rodents predisposes to poor fetal growth and interventions that enhance plasma volume expansion in FGR have shown beneficial effects on intrauterine fetal condition, prolongation of gestation and birth weight. This review makes the case for elevating the maternal intravascular volume with physical exercise with or without Nitric Oxide Donors in FGR and EPE, and evaluating its role as a potential target for prevention and/or management of these conditions.

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Section: Interactive Maternal-fetal Hemodynamics In Fetal Growth Rest...mentioning

confidence: 99%

Maternal Low Volume Circulation Relates to Normotensive and Preeclamptic Fetal Growth Restriction

Gyselaers

Lees

2022

Front. Med.

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“…There are several factors that resulted in PE, including a history of PE, chronic hypertension, pregestational diabetes mellitus, antiphospholipid syndrome, and obesity, among others (Bartsch et al, 2016). Recently, the dysfunction of placental trophoblast cells was considered as the key factor to trigger PE (Gyselaers et al, 2019). It has long been believed that inadequate transformation of the maternal uterine vasculature is a consequence of primary defective extravillous trophoblast cell invasion and leads to the development of PE (Ridder et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

lncRNA GHET1 regulates extravillous trophoblastic phenotype via EZH2/LSD1‐mediated MT2A epigenetic suppression in pre‐eclampsia

Wan

Huang

Liu

et al. 2023

Molecular Reproduction Devel

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Pre‐eclampsia (PE) is usually defined as new‐onset hypertension with albuminuria or other organ damage. Herein, the role and mechanism of long noncoding RNA (lncRNA) gastric carcinoma high expressed transcript 1 (GHET1) during PE are investigated. Expression of GHET1 in PE pregnancies was evaluated using quantitative real‐time polymerase chain reaction (qRT‐PCR). Proliferation and cell cycle of extravillous trophoblasts were assessed by Cell Counting Kit‐8 (CCK‐8), colony formation, 5‐Ethynyl‐2′‐deoxyuridine (EdU) assays, and flow cytometry, respectively. Migration, invasion, and network formation of trophoblasts were measured by wound healing, transwell system, and tube formation assays. RNA immunoprecipitation (RIP), RNA pull‐down, and chromatin immunoprecipitation (ChIP) assays were used to confirm the molecular interaction. GHET1 was markedly decreased in the placenta of PE patients. GHET1 promoted the proliferation and cell cycle of extravillous trophoblasts, as well as migration, invasion, and network formation in vitro. Metallothionein 2A (MT2A) functioned as a downstream effector of GHET1, which was negatively correlated with GHET1 in PE. GHET1 directly bound with zeste 2 polycomb repressive complex 2/lysine‐specific demethylase 1 (EZH2/LSD1). Knockdown of GHET1 reduced the occupancies of H3K27me3 and H3K4me2 in the MT2A promoter region by recruiting EZH2 and LSD1. MT2A knockdown reversed GHET1 inhibition mediated biological functions. GHET1 regulates extravillous trophoblastic phenotype via EZH2/LSD1‐mediated MT2A epigenetic suppression in PE.

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Prognosemodelle für Präeklampsie

Brezinka

2020

Gynäkologe

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Zusammenfassung Die Präeklampsie betrifft 3–5 % aller Schwangeren. Wurde bisher in der Schwangerenkontrolle mittels Blutdruckmessung, Achten auf das Auftreten von Ödemen und Proteinurie die Erkrankung im zweiten und dritten Trimenon durch ihre Prodrome und Symptome erkannt, stehen nun Prognosemodelle zur Verfügung. Mit diesen ist es möglich, bereits im ersten Trimenon ein erhöhtes Präeklampsierisiko festzustellen. Durch den Nachweis, dass die Gabe von Acetylsalicylsäure ab dem ersten Trimenon zu einer etwa 60 %igen Reduktion des Risikos für das Auftreten einer Präeklampsie führt, steht mit den Prognosemodellen ein schlüssiges Präventions- und Therapiekonzept zur Verfügung.

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Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries. Brosens I, Brosens JJ, Muter J, Puttemans P, Benagiano G. Am J Obstet Gynecol 2019;221:219-26.

Cited by 5 publications

References 4 publications

Maternal Low Volume Circulation Relates to Normotensive and Preeclamptic Fetal Growth Restriction

Maternal Low Volume Circulation Relates to Normotensive and Preeclamptic Fetal Growth Restriction

lncRNA GHET1 regulates extravillous trophoblastic phenotype via EZH2/LSD1‐mediated MT2A epigenetic suppression in pre‐eclampsia

Prognosemodelle für Präeklampsie

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