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Journal ArticleDOI

Comparative analysis of maternal-fetal interface in preeclampsia and preterm labor.

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TLDR
The results suggest that the maternal-fetal interface from cases of PTL without inflammation can be used for comparative purposes, e.g., as age-matched controls, in studies of the effects of PE on cells in this region.
Abstract
The maternal-fetal interface, a chimeric structure, is formed when fetal cytotrophoblasts (CTBs) from the placenta invade the uterine wall and its resident vasculature In preeclampsia (PE), interstitial and endovascular invasion are often shallow, and fewer spiral arterioles are breached in toto Our previous work has shown that faulty CTB differentiation to an invasive phenotype is a contributing factor Here, we have tested the hypothesis that the constellation of morphological and molecular defects that are associated with PE are unique to this condition Specifically, we have compared the histology of the maternal-fetal interface and CTB expression of stage-specific antigens in PE and in preterm labor (PTL) with or without inflammation In the absence of inflammation, biopsies obtained after PTL were near normal at histological and molecular levels In accord with previously published data, PE had severe negative effects on the endpoints analyzed Biopsies obtained after PTL with inflammation had an intermediate phenotype Our results suggest that the maternal-fetal interface from cases of PTL without inflammation can be used for comparative purposes, eg, as age-matched controls, in studies of the effects of PE on cells in this region

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Citations
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Journal ArticleDOI

Defective decidualization during and after severe preeclampsia reveals a possible maternal contribution to the etiology.

TL;DR: Evidence of a decidualization defect in the endometrium of women with severe preeclampsia (PE) that was detected at the time of delivery and persisted years after the affected pregnancy is provided to link this defect to impaired cytotrophoblast invasion.
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Severe Preeclampsia-Related Changes in Gene Expression at the Maternal-Fetal Interface Include Sialic Acid-Binding Immunoglobulin-Like Lectin-6 and Pappalysin-2

TL;DR: A global analysis of gene expression at the maternal-fetal interface in placental samples from women with PE and women who delivered due to preterm labor with no evidence of infection confirmed PE-related changes in the expression of Siglec-6 and PAPP-A2, which localized to invasive CTBs and syncytiotrophoblasts.
Journal ArticleDOI

A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

TL;DR: It is concluded that Notch signaling is crucial for TB vascular invasion in pre-eclampsia and in mouse placentas, as they play important roles in arterial differentiation/function.
Journal ArticleDOI

Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia

TL;DR: It is proposed that, in severe PE, the in vivo environment dysregulates CTB gene expression; the autocrine actions of the upregulated molecules (including SEMA3B) impair CTB differentiation, invasion and signaling; and patient-specific factors determine the signs.
Journal ArticleDOI

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations.

TL;DR: Comparison of the trophoblast subtype data within each group (severe preeclampsia or noninfected preterm birth) identified many highly differentially expressed genes, which suggested new avenues of investigation, in particular, the roles of PRG2, Kell blood group determinants, and urothelial cancer associated 1 in syncytiotrophoblast diseases.
References
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Journal ArticleDOI

Latest advances in understanding preeclampsia.

TL;DR: Recent work on the causes of preeclampsia is summarized, which reveals a new mode of maternal immune recognition of the fetus, relevant to the condition, and circulating factors derived from the placenta are now better understood.
Journal ArticleDOI

A united states national reference for fetal growth

TL;DR: The findings indicate that the prevalence of fetal growth restriction (FGR) will vary markedly, depending on the fetal growth curve used, and many previously published fetal growth curves no longer provide an up-to-date reference for describing the distribution of birth weight by gestational age.
Book

Pathology of the human placenta

TL;DR: Early development of the human placenta and histopathologic approach to villous alterations are studied.
Journal ArticleDOI

Preeclampsia: an endothelial cell disorder.

TL;DR: It is proposed that poorly perfused placental tissue releases a factor(s) into the systemic circulation that injuries endothelial cells and set in motion a dysfunctional cascade of coagulation, vasoconstriction, and intravascular fluid redistribution that results in the clinical syndrome of preeclampsia.
Journal ArticleDOI

Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants.

TL;DR: Findings point to a defect in the normal interaction between migratory trophoblast and maternal uterine tissues in pre‐eclampsia and in SGA, a feature not seen beyond the second trimester in normal pregnancy.
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