The role of extravillous trophoblasts and uterine NK cells in vascular remodeling during pregnancy

Wei, Xiao-Wei; Zhang, Yu-Chen; Wu, Fan; Tian, Fu‐Ju; Lin, Yi

doi:10.3389/fimmu.2022.951482

Cited by 16 publications

(3 citation statements)

References 155 publications

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“…These are branches of the uterine artery that will allow the adequate supply of nutrients and oxygen to the embryo. At the onset of placentation, uNKs promote a series of processes to transform these specific arteries, including: vessel dilatation, increased permeability, the progressive loss of endothelial cells, or phenotypic switching and migration of vascular smooth muscle cells [25][26][27] (Figure 1).…”

Section: The Role Of Natural Killer Cells In Early Pregnancymentioning

confidence: 99%

Maternal–Fetal Compatibility in Recurrent Pregnancy Loss

Cuadrado-Torroglosa,

García-Velasco,

Alecsandru

2024

JCM

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Nowadays, recurrent pregnancy loss (RPL) is an undesirable condition suffered by many patients of reproductive age. In this scenario, certain immune cell populations and molecules, involved in maternal–fetal compatibility, have emerged as factors related with the pathogenesis of RPL. Among them, uterine Natural Killer cells (uNKs) appear to be of great relevance. These cells are involved in numerous processes during pregnancy, such as the remodeling of uterine spiral arteries or the control of trophoblast invasion. These functions are regulated by the interactions that these cells establish with the extravillous trophoblast, mainly through their Killer Immunoglobulin-like Receptors (KIRs) and the Human Leukocyte Antigen-C (HLA-C) molecules expressed by the embryo. A high level of polymorphism has been reported for both molecules involved in this interaction, with some of the possible KIR–HLA-C combinations being associated with an increased risk of RPL. However, the complexity of the maternal–fetal interface goes beyond this, as other HLA molecules also appear to be related to this reproductive pathology. In this review, we will discuss the role of uNKs in pregnancy, as well as the polymorphisms and clinical implications of KIR–HLA-C binding. We will also address the involvement of other, different HLA molecules in RPL, and the current advice on the appropriate management of patients with ‘immunological mismatch’, thus covering the main aspects regarding the involvement of maternal–fetal compatibility in RPL.

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Section: The Role Of Natural Killer Cells In Early Pregnancymentioning

confidence: 99%

Maternal–Fetal Compatibility in Recurrent Pregnancy Loss

Cuadrado-Torroglosa,

García-Velasco,

Alecsandru

2024

JCM

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“…The two-stage process of implantation and placental development involves maternal–fetal interaction and adaptation [ 53 , 54 ]. The changes in the syncytiotrophoblast, trophoblast, and uterine arteries are under the influence of uterine natural killer cells and regulatory T cells [ 55 , 56 ]. Angiogenic factors, such as the PlGF (placental growth factor) and sFLT (soluble fms-like tyrosine kinase-1) regulate placental angioneogenesis, vasculogenesis, and maternal circulatory adaption [ 57 ].…”

Section: Placenta-related Syndromesmentioning

confidence: 99%

Evaluating Current Molecular Techniques and Evidence in Assessing Microbiome in Placenta-Related Health and Disorders in Pregnancy

Stupak

Kwaśniewski

2023

Biomolecules

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The microbiome is of great interest due to its potential influence on the occurrence and treatment of some human illnesses. It may be regarded as disruptions to the delicate equilibrium that humans ordinarily maintain with their microorganisms or the microbiota in their environment. The focus of this review is on the methodologies and current understanding of the functional microbiome in pregnancy outcomes. We present how novel techniques bring new insights to the contemporary field of maternal–fetal medicine with a critical analysis. The maternal microbiome in late pregnancy has been extensively studied, although data on maternal microbial changes during the first trimester are rare. Research has demonstrated that, in healthy pregnancies, the origin of the placental microbiota is oral (gut) rather than vaginal. Implantation, placental development, and maternal adaptation to pregnancy are complex processes in which fetal and maternal cells interact. Microbiome dysbiosis or microbial metabolites are rising as potential moderators of antenatal illnesses related to the placenta, such as fetal growth restriction, preeclampsia, and others, including gestational diabetes and preterm deliveries. However, because of the presence of antimicrobial components, it is likely that the bacteria identified in placental tissue are (fragments of) bacteria that have been destroyed by the placenta’s immune cells. Using genomic techniques (metagenomics, metatranscriptomics, and metaproteomics), it may be possible to predict some properties of a microorganism’s genome and the biochemical (epigenetic DNA modification) and physical components of the placenta as its environment. Despite the results described in this review, this subject needs further research on some major and crucial aspects. The phases of an in utero translocation of the maternal gut microbiota to the fetus should be explored. With a predictive knowledge of the impacts of the disturbance on microbial communities that influence human health and the environment, genomics may hold the answer to the development of novel therapies for the health of pregnant women.

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“…It is well known that trophoblast cells are the origin of sFLT1 that enters the maternal circulation during pregnancy, leading to the hypothesis that abnormal trophoblast formation and therefore excess sFLT1 is the primary cause of maternal vascular dysfunction in this disease through its sequestration of VEGF [10]. Abnormal trophoblast invasion into the maternal decidua has been intensely studied in PE [11]. A recent single-cell transcriptomic study in human pregnancy revealed a cell-autonomous dysregulation of FLT1 and PLGF transcription in the syncytial trophoblast in early but not late preeclampsia [12].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice

Vogtmann,

Riedel,

Sassmannshausen

et al. 2024

IJMS

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Preeclampsia (PE) is characterized by maternal hypertension and placental dysfunction, often leading to fetal growth restriction (FGR). It is associated with an overexpression of the anti-angiogenic sFLT1 protein, which originates from the placenta and serves as a clinical biomarker to predict PE. To analyze the impact of sFLT1 on placental function and fetal growth, we generated transgenic mice with placenta-specific human sFLT1 (hsFLT1) overexpression. Immunohistochemical, morphometrical, and molecular analyses of the placentas on 14.5 dpc and 18.5 dpc were performed with a focus on angiogenesis, nutrient transport, and inflammation. Additionally, fetal development upon placental hsFLT1 overexpression was investigated. Dams exhibited a mild increase in serum hsFLT1 levels upon placental hsFLT1 expression and revealed growth restriction of the fetuses in a sex-specific manner. Male FGR fetuses expressed higher amounts of placental hsFLT1 mRNA compared to females. FGR placentas displayed an altered morphology, hallmarked by an increase in the spongiotrophoblast layer and changes in labyrinthine vascularization. Further, FGR placentas showed a significant reduction in placental glycogen storage and nutrient transporter expression. Moreover, signs of hypoxia and inflammation were observed in FGR placentas. The transgenic spongiotrophoblast-specific hsFLT1 mouse line demonstrates that low hsFLT1 serum levels are sufficient to induce significant alterations in fetal and placental development in a sex-specific manner.

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The role of extravillous trophoblasts and uterine NK cells in vascular remodeling during pregnancy

Cited by 16 publications

References 155 publications

Maternal–Fetal Compatibility in Recurrent Pregnancy Loss

Maternal–Fetal Compatibility in Recurrent Pregnancy Loss

Evaluating Current Molecular Techniques and Evidence in Assessing Microbiome in Placenta-Related Health and Disorders in Pregnancy

Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice

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