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Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular...
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Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular Mechanisms

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 6145

Special Issue Editors

Prof. Dr. Andrea Hartner

E-Mail Website
Guest Editor
Department of Pediatrics and Adolescent Medicine, University Hospital of Erlangen, 91054 Erlangen, Germany
Interests: perinatal programming; cardiovascular and renal consequences; organ fibrosis
Dr. Fabian B. Fahlbusch

E-Mail Website
Guest Editor
Department of Pediatrics and Adolescent Medicine, University Hospital of Erlangen, 91054 Erlangen, Germany
Interests: placenta; developmental origins of health and disease; perinatology

Special Issue Information

Dear Colleagues,

Intrauterine growth restriction (IUGR), or fetal growth restriction (FGR), describes a pathological condition in which the fetus fails to grow to its biological potential. This condition is often associated with preeclampsia (PE). These adverse pregnancy outcomes (APO) entail the risk of prematurity and PE negatively affects the maternal cardiovascular system even after delivery. Furthermore, the current state of research under the developmental origins of health and disease (DOHaD) theorem indicates that an unfavorable intrauterine environment leads to “fetal programming” with short- and long-term health consequences. These include metabolic, cardiovascular, renal, immunological, and neurological disease, all associated with a relevant health burden. Unfortunately, the underlying cellular and molecular mechanisms causing placental dysfunction and altering fetal/offspring organ development remain largely unknown, with a subsequent lack of adequate screening approaches and therapeutic tools. Therefore, we cordially invite all scientists in the field of fetal, placental, and maternal health working on the origin and the consequences of IUGR or IUGR/PE to participate in this Special Issue, moving the bench closer to the bedside.

Original research articles, reviews, or shorter perspective articles on all aspects related to the molecular and cellular mechanisms of the biology and therapy of these APOs are welcome. Articles with insights from a cellular and molecular biological perspective are especially welcome. Relevant topics include but are not limited to: feto-maternal crosstalk, metabolomics, endocrinology, animal models, primary cell cultures, placenta, fetal and postnatal organ development, genetic and epigenetic profiles, molecular and cellular heterogeneity, and any other topics related to the molecular and cellular etiopathogenesis and sequelae of IUGR and IUGR/PE.

Prof. Dr. Andrea Hartner
Dr. Fabian B. Fahlbusch
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • IUGR
  • PE
  • mechanisms
  • consequences
  • origins

Published Papers (4 papers)

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Research

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14 pages, 2088 KiB  
Article
Angiogenic Function of Human Placental Endothelial Cells in Severe Fetal Growth Restriction Is Not Rescued by Individual Extracellular Matrix Proteins
by Lauren Sayres, Amanda R. Flockton, Shuhan Ji, Carla Rey Diaz, Diane L. Gumina and Emily J. Su
Cells 2023, 12(19), 2339; https://doi.org/10.3390/cells12192339 - 23 Sep 2023
Viewed by 820
Abstract
Severe fetal growth restriction (FGR) is characterized by increased placental vascular resistance resulting from aberrant angiogenesis. Interactions between endothelial cells (ECs) and the extracellular matrix (ECM) are critical to the complex process of angiogenesis. We have previously found that placental stromal abnormalities contribute [...] Read more.
Severe fetal growth restriction (FGR) is characterized by increased placental vascular resistance resulting from aberrant angiogenesis. Interactions between endothelial cells (ECs) and the extracellular matrix (ECM) are critical to the complex process of angiogenesis. We have previously found that placental stromal abnormalities contribute to impaired angiogenesis in severe FGR. The objective of this research is to better characterize the effect of individual ECM proteins on placental angiogenic properties in the setting of severe FGR. ECs were isolated from human placentae, either control or affected by severe FGR, and subjected to a series of experiments to interrogate the role of ECM proteins on adhesion, proliferation, migration, and apoptosis. We found impaired proliferation and migration of growth-restricted ECs. Although individual substrates did not substantially impact migratory capacity, collagens I, III, and IV partially mitigated proliferative defects seen in FGR ECs. Differences in adhesion and apoptosis between control and FGR ECs were not evident. Our findings demonstrate that placental angiogenic defects that characterize severe FGR cannot be explained by a singular ECM protein, but rather, the placental stroma as a whole. Further investigation of the effects of stromal composition, architecture, stiffness, growth factor sequestration, and capacity for remodeling is essential to better understand the role of ECM in impaired angiogenesis in severe FGR. Full article
(This article belongs to the Special Issue Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular Mechanisms)
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22 pages, 3867 KiB  
Article
Altered Cord Blood Lipid Concentrations Correlate with Birth Weight and Doppler Velocimetry of Fetal Vessels in Human Fetal Growth Restriction Pregnancies
by Stephanie S. Chassen, Karin Zemski-Berry, Stefanie Raymond-Whish, Camille Driver, John C. Hobbins and Theresa L. Powell
Cells 2022, 11(19), 3110; https://doi.org/10.3390/cells11193110 - 02 Oct 2022
Cited by 6 | Viewed by 1912
Abstract
Fetal growth restriction (FGR) is associated with short- and long-term morbidity, often with fetal compromise in utero, evidenced by abnormal Doppler velocimetry of fetal vessels. Lipids are vital for growth and development, but metabolism in FGR pregnancy, where fetuses do not grow to [...] Read more.
Fetal growth restriction (FGR) is associated with short- and long-term morbidity, often with fetal compromise in utero, evidenced by abnormal Doppler velocimetry of fetal vessels. Lipids are vital for growth and development, but metabolism in FGR pregnancy, where fetuses do not grow to full genetic potential, is poorly understood. We hypothesize that triglyceride concentrations are increased in placentas and that important complex lipids are reduced in cord plasma from pregnancies producing the smallest babies (birth weight < 5%) and correlate with ultrasound Dopplers. Dopplers (umbilical artery, UA; middle cerebral artery, MCA) were assessed longitudinally in pregnancies diagnosed with estimated fetal weight (EFW) < 10% at ≥29 weeks gestation. For a subset of enrolled women, placentas and cord blood were collected at delivery, fatty acids were extracted and targeted lipid class analysis (triglyceride, TG; phosphatidylcholine, PC; lysophosphatidylcholine, LPC; eicosanoid) performed by LCMS. For this sub-analysis, participants were categorized as FGR (Fenton birth weight, BW ≤ 5%) or SGA “controls” (Fenton BW > 5%). FGRs (n = 8) delivered 1 week earlier (p = 0.04), were 29% smaller (p = 0.002), and had 133% higher UA pulsatility index (PI, p = 0.02) than SGAs (n = 12). FGR plasma TG, free arachidonic acid (AA), and several eicosanoids were increased (p < 0.05); docosahexaenoic acid (DHA)-LPC was decreased (p < 0.01). Plasma TG correlated inversely with BW (p < 0.05). Plasma EET, non-esterified AA, and DHA correlated inversely with BW and directly with UA PI (p < 0.05). Placental DHA-PC and AA-PC correlated directly with MCA PI (p < 0.05). In fetuses initially referred for inadequate fetal growth (EFW < 10%), those with BW ≤ 5% demonstrated distinctly different cord plasma lipid profiles than those with BW > 5%, which correlated with Doppler PIs. This provides new insights into fetal lipidomic response to the FGR in utero environment. The impact of these changes on specific processes of growth and development (particularly fetal brain) have not been elucidated, but the relationship with Doppler PI may provide additional context for FGR surveillance, and a more targeted approach to nutritional management of these infants. Full article
(This article belongs to the Special Issue Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular Mechanisms)
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Review

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11 pages, 1123 KiB  
Review
From Molecules to Imaging: Assessment of Placental Hypoxia Biomarkers in Placental Insufficiency Syndromes
by Fatimah M. Al Darwish, Lotte Meijerink, Bram F. Coolen, Gustav J. Strijkers, Mireille Bekker, Titia Lely and Fieke Terstappen
Cells 2023, 12(16), 2080; https://doi.org/10.3390/cells12162080 - 17 Aug 2023
Viewed by 1350
Abstract
Placental hypoxia poses significant risks to both the developing fetus and the mother during pregnancy, underscoring the importance of early detection and monitoring. Effectively identifying placental hypoxia and evaluating the deterioration in placental function requires reliable biomarkers. Molecular biomarkers in placental tissue can [...] Read more.
Placental hypoxia poses significant risks to both the developing fetus and the mother during pregnancy, underscoring the importance of early detection and monitoring. Effectively identifying placental hypoxia and evaluating the deterioration in placental function requires reliable biomarkers. Molecular biomarkers in placental tissue can only be determined post-delivery and while maternal blood biomarkers can be measured over time, they can merely serve as proxies for placental function. Therefore, there is an increasing demand for non-invasive imaging techniques capable of directly assessing the placental condition over time. Recent advancements in imaging technologies, including photoacoustic and magnetic resonance imaging, offer promising tools for detecting and monitoring placental hypoxia. Integrating molecular and imaging biomarkers may revolutionize the detection and monitoring of placental hypoxia, improving pregnancy outcomes and reducing long-term health complications. This review describes current research on molecular and imaging biomarkers of placental hypoxia both in human and animal studies and aims to explore the benefits of an integrated approach throughout gestation. Full article
(This article belongs to the Special Issue Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular Mechanisms)
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Other

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9 pages, 1308 KiB  
Perspective
Hyperglycosylated-hCG: Its Role in Trophoblast Invasion and Intrauterine Growth Restriction
by Catalin Gabriel Herghelegiu, Alina Veduta, Miruna Florina Stefan, Stefania Lucia Magda, Iuliana Ionascu, Viorica Elena Radoi, Daniela Nuti Oprescu and Alina Mihaela Calin
Cells 2023, 12(12), 1647; https://doi.org/10.3390/cells12121647 - 16 Jun 2023
Cited by 1 | Viewed by 1386
Abstract
Human chorionic gonadotropin (hCG) is produced by the placenta and its roles have been studied for over a century, being the first known pregnancy-related protein. Although its main role is to stimulate the production of progesterone by corpus luteal cells, hCG does not [...] Read more.
Human chorionic gonadotropin (hCG) is produced by the placenta and its roles have been studied for over a century, being the first known pregnancy-related protein. Although its main role is to stimulate the production of progesterone by corpus luteal cells, hCG does not represent just one biologically active molecule, but a group of at least five variants, produced by different cells and each with different functions. The hyperglycosylated variant of hCG (H-hCG) plays a key role in trophoblast invasion, placental development and fetal growth. During trophoblast invasion, H-hCG promotes extravillous cytotrophoblast cells to infiltrate the decidua, and also to colonize and remodel the spiral arteries in to low resistance, larger-diameter vessels. As fetal growth is heavily reliant on nutrient availability, impaired trophoblast invasion and remodeling of the uterine arteries, leads to a defective perfusion of the placenta and fetal growth restriction. Understanding the function of H-hCG in the evolution of the placenta might unveil new ways to manage and treat fetal growth restriction. Full article
(This article belongs to the Special Issue Etiopathogenesis and Sequelae of Intrauterine Growth Restriction: Cellular and Molecular Mechanisms)
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