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Cells
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Molecular and Cellular Mechanisms of Fetal Growth and Preterm Birth
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Molecular and Cellular Mechanisms of Fetal Growth and Preterm Birth

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 5083

Special Issue Editor

Dr. Vasilios Pergialiotis

E-Mail Website
Guest Editor
1st Department of Obstetrics and Gynecology, National and Kapodistrian University of Athens, Alexandra Hospital, 11528 Athens, Greece
Interests: meta-analysis; laparoscopic surgery; cohort studies; obstetric delivery; gynaecological surgery screening; fetal growth restriction; prenatal diagnosis; proteomics; reproductive medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will provide an in-depth overview of our current knowledge on molecular and cellular mechanisms that promote fetal growth, with a special interest in transcriptional and post-transcriptional factors associated with preterm birth. Several mechanisms have been implicated in the pathophysiology of preterm birth, including infectious factors, mechanical factors as well as genetic and epigenetic modifications. It has recently been suggested that there is a complex interplay regulating the processes that precede the onset of preterm birth.

In this Special Issue of Cells, we seek contributions in the form of original research articles, reviews, or shorter perspective articles on all aspects related to the subject of “Molecular and cellular mechanisms of fetal growth and preterm birth”. Potential topics include, but are not limited to, the following: genetic and epigenetic factors of fetal growth and preterm birth, molecular and cellular mechanisms involved in infectious morbidity that precedes preterm birth, DNA methylation, RNA methylation, miRNA regulation, and histone modification in preterm birth. In the present Issue, we hope that leading experts will share their perspectives on the pathophysiology of preterm birth and will contribute to the current knowledge with novel evidence that provides the foundation for further research.

Dr. Vasilios Pergialiotis
Guest Editor

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.

Published Papers (3 papers)

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Research

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12 pages, 1163 KiB  
Communication
Expression of Stemness Markers in the Cervical Smear of Patients with Cervical Insufficiency
by Savvia Pittokopitou, Despina Mavrogianni, Vasilios Pergialiotis, Kalliopi I. Pappa, Panagiotis Antsaklis, Marianna Theodora, Michail Sindos, Angeliki Papapanagiotou, Aikaterini Domali, Sofoklis Stavros, Peter Drakakis and George Daskalakis
Cells 2023, 12(8), 1183; https://doi.org/10.3390/cells12081183 - 18 Apr 2023
Viewed by 1102
Abstract
The presence of stem cells has been previously described in human precancerous and malignant cervical cultures. Previous studies have shown a direct interplay of the stem cell niche, which is present in practically every tissue with the extracellular matrix. In the present study, [...] Read more.
The presence of stem cells has been previously described in human precancerous and malignant cervical cultures. Previous studies have shown a direct interplay of the stem cell niche, which is present in practically every tissue with the extracellular matrix. In the present study, we sought to determine the expression of stemness markers in cytological specimens collected from the ectocervix among women with cervical insufficiency during the second trimester of pregnancy and women with normal cervical length. A prospective cohort of 59 women was enrolled of whom 41 were diagnosed with cervical insufficiency. The expression of OCT-4 and NANOG was higher in the cervical insufficiency group compared to the control group (−5.03 (−6.27, −3.72) vs. −5.81 (−7.67, −5.02) p = 0.040 for OCT4) and (−7.47 (−8.78, −6.27) vs. −8.5 (−10.75, −7.14), p = 0.035 for NANOG. Differences in the DAZL gene were not significantly different (5.94 (4.82, 7.14) vs. 6.98 (5.87, 7.43) p = 0.097). Pearson correlation analysis indicated the existence of a moderate correlation of OCT-4 and Nanog with cervical length. Considering this information, the enhanced activity of stemness biomarkers among pregnant women diagnosed with cervical insufficiency may be predisposed to cervical insufficiency, and its predictive accuracy remains to be noted in larger population sizes. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Fetal Growth and Preterm Birth)
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17 pages, 2796 KiB  
Article
Integrated Placental Modelling of Histology with Gene Expression to Identify Functional Impact on Fetal Growth
by Hannah Ee Juen Yong, Katarzyna Maksym, Muhammad Ashraf Bin Yusoff, Esteban Salazar-Petres, Tatiana Nazarenko, Alexey Zaikin, Anna L. David, Sara L. Hillman and Amanda N. Sferruzzi-Perri
Cells 2023, 12(7), 1093; https://doi.org/10.3390/cells12071093 - 06 Apr 2023
Cited by 2 | Viewed by 1823
Abstract
Fetal growth restriction (FGR) is a leading cause of perinatal morbidity and mortality. Altered placental formation and functional capacity are major contributors to FGR pathogenesis. Relating placental structure to function across the placenta in healthy and FGR pregnancies remains largely unexplored but could [...] Read more.
Fetal growth restriction (FGR) is a leading cause of perinatal morbidity and mortality. Altered placental formation and functional capacity are major contributors to FGR pathogenesis. Relating placental structure to function across the placenta in healthy and FGR pregnancies remains largely unexplored but could improve understanding of placental diseases. We investigated integration of these parameters spatially in the term human placenta using predictive modelling. Systematic sampling was able to overcome heterogeneity in placental morphological and molecular features. Defects in villous development, elevated fibrosis, and reduced expression of growth and functional marker genes (IGF2, VEGA, SLC38A1, and SLC2A3) were seen in age-matched term FGR versus healthy control placentas. Characteristic histopathological changes with specific accompanying molecular signatures could be integrated through computational modelling to predict if the placenta came from a healthy or FGR pregnancy. Our findings yield new insights into the spatial relationship between placental structure and function and the etiology of FGR. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Fetal Growth and Preterm Birth)
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Review

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7 pages, 255 KiB  
Review
Inflammatory Molecules Responsible for Length Shortening and Preterm Birth
by Zacharias Fasoulakis, Antonios Koutras, Thomas Ntounis, Panos Antsaklis, Marianna Theodora, Asimina Valsamaki, George Daskalakis and Emmanuel N. Kontomanolis
Cells 2023, 12(2), 209; https://doi.org/10.3390/cells12020209 - 04 Jan 2023
Cited by 2 | Viewed by 1697
Abstract
It is estimated that inflammation at the placental–maternal interface is directly responsible for or contributes to the development of 50% of all premature deliveries. Chorioamnionitis, also known as the premature rupture of the amniotic membrane in the mother, is the root cause of [...] Read more.
It is estimated that inflammation at the placental–maternal interface is directly responsible for or contributes to the development of 50% of all premature deliveries. Chorioamnionitis, also known as the premature rupture of the amniotic membrane in the mother, is the root cause of persistent inflammation that preterm newborns experience. Beyond contributing to the onset of early labor, inflammation is a critical element in advancing several conditions in neonates, including necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, intraventricular hemorrhage, retinopathy of prematurity and periventricular leukomalacia. Notably, the immune systems of preterm infants are not fully developed; immune defense mechanisms and immunosuppression (tolerance) have a delicate balance that is easily upset in this patient category. As a result, premature infants are exposed to different antigens from elements such as hospital-specific microbes, artificial devices, medications, food antigens and hypoxia/hyperoxia. This has detrimental implications for preterm deliveries of less than 28 weeks because they have not yet evolved the mechanisms to tolerate maternal and self-antigens. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Fetal Growth and Preterm Birth)
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