scholarly journals Trophoblast-derived hyaluronan promotes the regulatory phenotype of decidual macrophages

Reproduction ◽  
2019 ◽  
pp. 189-198 ◽  
Author(s):  
Songcun Wang ◽  
Fengrun Sun ◽  
Mutian Han ◽  
Yinghua Liu ◽  
Qinyan Zou ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Signaling Pathways ◽  
Fetal Growth ◽  
Pregnancy Complications ◽  
Fetal Growth Restriction ◽  
Normal Pregnancy ◽  
M2 Polarization ◽  
Inflammatory Molecule ◽  
Regulatory Phenotype ◽  
Maternal Fetal Interface

There is delicate crosstalk between fetus-derived trophoblasts (Tros) and maternal cells during normal pregnancy. Dysfunctions in interaction are highly linked to some pregnancy complications, such as recurrent spontaneous abortion (RSA), pre-eclampsia and fetal growth restriction. Hyaluronan (HA), the most abundant component of extracellular matrix, has been reported to act as both a pro- and an anti-inflammatory molecule. Previously, we reported that HA promotes the invasion and proliferation of Tros by activating PI3K/Akt and MAPK/ERK1/2 signaling pathways. While lower HA secretion by Tros was observed during miscarriages than that during normal pregnancies, in the present study, we further confirmed that higher secretion of HA by Tros could induce M2 polarization of macrophages at the maternal–fetal interface by interacting with CD44 and activating the downstream PI3K/Akt-STAT-3/STAT-6 signaling pathways. Furthermore, HA could restore the production of IL-10 and other normal pregnancy markers by decidual macrophages (dMφs) from RSA. These findings underline the important roles of HA in regulating the function of dMφs and maintaining a normal pregnancy.

Toll-like Receptors at the Maternal-Fetal Interface in Normal Pregnancy and Pregnancy Complications

2014 ◽  
Vol 72 (2) ◽  
pp. 192-205 ◽  
Author(s):  
Kaori Koga ◽  
Gentaro Izumi ◽  
Gil Mor ◽  
Tomoyuki Fujii ◽  
Yutaka Osuga
Keyword(s):  
Pregnancy Complications ◽  
Normal Pregnancy ◽  
Toll Like Receptors ◽  
Maternal Fetal Interface

Umbilical artery extracellular matrix remodeling in fetal growth restriction

2004 ◽  
Vol 191 (6) ◽  
pp. S10
Author(s):  
Wendy Kinzler ◽  
John Smulian ◽  
C. Andrew Kistler ◽  
Rita Hahn ◽  
Peihong Zhou ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Umbilical Artery ◽  
Growth Restriction ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

scholarly journals The Role of HLAC and NK Cells in Fetal Growth Restriction

2017 ◽  
pp. 142
Author(s):  
Sri Sulistyawati ◽  
Didon M Trimulya ◽  
Supriyadi H Respati ◽  
Soetrisno Soetrisno
Keyword(s):  
Nk Cells ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Nk Cell ◽  
Normal Pregnancy ◽  
Growth Restriction ◽  
Immunohistochemical Method ◽  
Cross Sectional ◽  
The Mean

Objective: To determine the role of HLA-C and NK cell expressions in fetal growth restriction (FGR). Methods: A cross sectional study design was used. This study was conducted at the Obstetrics and Gynecology Department of Dr. Moewardi General Hospital, Surakarta, its affiliated hospitals, and at the Pathological Anatomy Laboratory of the Faculty of Medicine, University of Sebelas Maret Surakarta. A total of 40 samples were included in this study. The samples consisted of 20 normal pregnancies and 20 pregnancies with FGR. HLA-C expression in the trophoblast and NK cells in decidua of the subjects who met the inclusion and exclusion criteria were examined using immunohistochemical method and statistical analysis with T test. Results: The mean expression of HLA-C in the trophoblast in the pregnant group with FGR was 9.021.30, normal pregnancy was 7.96 ± 0.97, p=0.01 (p<0.05). The mean expression of NK cells in decidua of pregnancy with FGR was 10.59 ± 2.11, normal pregnancy was 0.91 ± 8.18, with p=0.00 (p<0.05). Conclusion: The expressions of HLA-C in trophoblast and NK cells in decidua of pregnancy with FGR were higher compared with those of normal pregnancy. [Indones J Obstet Gynecol 2017; 5-3: 142-148] Keywords: fetal growth restriction, HLA-C, NK cells

Characterization of fetal monocytes in preeclampsia and fetal growth restriction

2019 ◽  
Vol 47 (4) ◽  
pp. 434-438 ◽  
Author(s):  
Thushari I. Alahakoon ◽  
Heather Medbury ◽  
Helen Williams ◽  
Nicole Fewings ◽  
Xin M. Wang ◽  
...  
Keyword(s):  
Cord Blood ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Normal Pregnancy ◽  
Growth Restriction ◽  
Clinical Group ◽  
Monocyte Subset ◽  
Maternal Circulation ◽  
Cross Sectional ◽  
And Function

AbstractBackgroundThere is little available data on fetal monocyte phenotype and function. A prospective cross-sectional pilot study was conducted to describe the cord blood monocyte subset phenotype in preeclampsia (PE) and fetal growth restriction (FGR) as compared to normal pregnancy and maternal circulation.MethodsMaternal and cord blood samples from 27 pregnancies were collected at delivery from normal pregnancy, PE, FGR and PE+FGR. The distribution of fetal monocyte subtypes was characterized by CD14 and CD16 expression using flow cytometry and compared for each clinical group using a classification of classical, intermediate and non-classical subsets.ResultsThe intermediate monocytes were the dominant monocyte subset in the cord blood of PE and PE+FGR with an increase in the combined inflammatory monocyte subsets intermediate and non-classical in PE compared to normal pregnancy. The non-classical monocyte subset proportion was elevated in all pathological groups PE, FGR and PE+FGR. A significant reduction in the non-classical monocyte subset was observed in the cord blood of the normal pregnancy group as compared to the maternal circulation.ConclusionThis study describes for the first time in the fetal circulation, dominant monocyte intermediate subsets and increased inflammatory subsets in PE as well as increased non-classical subsets in PE and FGR compared to normal pregnancy.

scholarly journals Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia

2014 ◽  
Vol 211 (1) ◽  
pp. 165-179 ◽  
Author(s):  
Tiziana Cotechini ◽  
Maria Komisarenko ◽  
Arissa Sperou ◽  
Shannyn Macdonald-Goodfellow ◽  
Michael A. Adams ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Pregnancy Complications ◽  
Fetal Growth Restriction ◽  
Nitrosative Stress ◽  
Growth Restriction ◽  
Trophoblast Invasion ◽  
Spiral Artery ◽  
Transdermal Administration ◽  
Pregnant Rats ◽  
Maternal Inflammation

Fetal growth restriction (FGR) and preeclampsia (PE) are often associated with abnormal maternal inflammation, deficient spiral artery (SA) remodeling, and altered uteroplacental perfusion. Here, we provide evidence of a novel mechanistic link between abnormal maternal inflammation and the development of FGR with features of PE. Using a model in which pregnant rats are administered low-dose lipopolysaccharide (LPS) on gestational days 13.5–16.5, we show that abnormal inflammation resulted in FGR mediated by tumor necrosis factor-α (TNF). Inflammation was also associated with deficient trophoblast invasion and SA remodeling, as well as with altered uteroplacental hemodynamics and placental nitrosative stress. Moreover, inflammation increased maternal mean arterial pressure (MAP) and was associated with renal structural alterations and proteinuria characteristic of PE. Finally, transdermal administration of the nitric oxide (NO) mimetic glyceryl trinitrate prevented altered uteroplacental perfusion, LPS-induced inflammation, placental nitrosative stress, renal structural and functional alterations, increase in MAP, and FGR. These findings demonstrate that maternal inflammation can lead to severe pregnancy complications via a mechanism that involves increased maternal levels of TNF. Our study provides a rationale for the use of antiinflammatory agents or NO-mimetics in the treatment and/or prevention of inflammation-associated pregnancy complications.

OP22.09: Placental T2*in normal pregnancy and in two cases of fetal growth restriction

2014 ◽  
Vol 44 (S1) ◽  
pp. 165-166 ◽  
Author(s):  
M. Sinding ◽  
A. Sørensen ◽  
D. Peters ◽  
E. Hoseth ◽  
C. Simonsen ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Normal Pregnancy ◽  
Growth Restriction

scholarly journals OR24-07 Fetal Sex Impacts First Trimester Maternal-Fetal Communication in Humans

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tania L Gonzalez ◽  
Tianyanxin Sun ◽  
Nan Deng ◽  
Rosemarie DiPentino ◽  
Ekaterina L Clark ◽  
...  
Keyword(s):  
Single Cell ◽  
Signaling Pathways ◽  
Rna Sequencing ◽  
Fetal Growth ◽  
Individual Cell ◽  
Cell Types ◽  
First Trimester ◽  
Sexually Dimorphic ◽  
Upstream Regulator ◽  
Maternal Fetal Interface

Abstract The placenta serves as a regulator of fetal growth throughout pregnancy. Signaling at the maternal-fetal interface is critical during placentation and lays the groundwork for placenta function, affecting pregnancy outcomes. Fetal growth is impacted by fetal sex, with males larger than females, and maternal gestational diabetes and obesity independently increase the risk of macrosomia in male fetuses only. We previously demonstrated differentially expressed genes (DEGs) among sexes involves ancient canonical pathways and metabolic functions in placenta tissue. As these are likely impacted by signaling at the maternal-fetal interface, our aim here was to identify sex differences in signaling at the maternal-fetal interface and among individual cell types within the placenta to explain these differences. RNA-sequencing of first trimester placenta and maternal decidua as well as single cell RNA-sequencing in first trimester placenta was performed in ongoing pregnancies. We identified 91 sexually dimorphic receptor-ligand pairs across the maternal-fetal interface. From these, 35 of 115 receptors and/or ligand genes were also found to be upstream regulators of pathways critical in sexually dimorphic placentation which may define regulation. Single cell analysis identified five major cell types (trophoblasts, stromal cells, hofbauer cells, antigen presenting cells, and endothelial cells), and all had sexually dimorphic genes. Among individual cell types, ligands from the CC-family of cytokines were most highly representative in females, with their corresponding receptors present on the maternal surface. Furthermore, upstream regulator analysis of sexually dimorphic genes demonstrated TGFβ1 and estradiol to significantly affect all cell types. Dihydrotestosterone, which is produced by the male fetus, was an upstream regulator that was most significant for the trophoblast population. In addition, gene ontology enrichment analysis identified distinctive enriched functions between male and female trophoblasts, with cytokine mediated signaling pathways most representative. MUC15 and NOTUM were the most highly expressed sexually dimorphic autosomal genes found in distinct cell types of the trophoblast population, cell types critical for placentation and nutrient exchange. Thus, differences in hormone and immune signaling pathways may account for differential gene expression and differences in trophoblast function during placentation, which may in turn explain developmental differences, including fetal size, well-being, and overall outcomes.

scholarly journals 11β-Hydroxysteroid Dehydrogenase 2 in Preeclampsia

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Katarzyna Kosicka ◽  
Anna Siemiątkowska ◽  
Franciszek K. Główka
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Placental Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Normal Pregnancy ◽  
Medical Problem ◽  
Growth Restriction ◽  
Research Projects ◽  
Reduced Activity ◽  
The Way

Preeclampsia is a serious medical problem affecting the mother and her child and influences their health not only during the pregnancy, but also many years after. Although preeclampsia is a subject of many research projects, the etiology of the condition remains unclear. One of the hypotheses related to the etiology of preeclampsia is the deficiency in placental 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2), the enzyme which in normal pregnancy protects the fetus from the excess of maternal cortisol. The reduced activity of the enzyme was observed in placentas from pregnancies complicated with preeclampsia. That suggests the overexposure of the developing child to maternal cortisol, which in high levels exerts proapoptotic effects and reduces fetal growth. The fetal growth restriction due to the diminished placental 11β-HSD2 function may be supported by the fact that preeclampsia is often accompanied with fetal hypotrophy. The causes of the reduced function of 11β-HSD2 in placental tissue are still discussed. This paper summarizes the phenomena that may affect the activity of the enzyme at various steps on the way from the gene to the protein.

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