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Life
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New Insights into the Placental and Placental Membrane Pathophysiology of...
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New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth Version 2.0

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Reproductive and Developmental Biology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 1189

Special Issue Editor

Dr. Chan-Wook Park

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
Interests: preterm birth; preterm labor; preterm-PROM; fetal growth restriction; placenta; feto-maternal interface; ascending intrauterine infection; intra-amniotic inflammation; chorioamnionitis; maternal vascular malperfusion; fetal vascular malperfusion; neonatal morbidity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Preterm birth is a leading cause of perinatal morbidity and mortality. Unfortunately, preterm births continue unabated despite the rapid progress of medical science. To resolve this matter for the future, it is essential to determine the exact pathophysiology of the placenta in preterm birth. 

Preterm birth is divided into spontaneous preterm birth (due to preterm labor and intact membranes and the preterm premature rupture of membranes) and indicated preterm birth (due to preeclampsia and idiopathic fetal growth restriction). Ascending intrauterine infection and subsequent acute histologic chorioamnionitis (i.e., a maternal inflammatory response in the placenta; inflammation in extraplacental membranes and the chorionic plate) and/or fetal inflammation (i.e., a fetal inflammatory response in the placenta; inflammation in the umbilical cord and chorionic vessels) are known to be among the central pathophysiologies in spontaneous preterm birth. 

Utero–placental insufficiency (i.e., maternal vascular malperfusion and fetal vascular malperfusion in the placenta) is an important pathophysiology in preeclampsia and idiopathic fetal growth restriction. 

Meticulous research on the histopathology and molecular pathology (i.e., immunohistochemistry and transcriptomic analysis) in the placenta and placental membrane of preterm birth will provide us with the basis for the prevention and treatment of numerous patients at risk of preterm birth.

This Special Issue aims to present new insights in the field, covering areas ranging from histopathology to molecular pathology in the placenta and placental membrane of preterm birth. We welcome original research articles and reviews on the placental pathophysiology of preterm birth.

Dr. Chan-Wook Park
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. Life is an international peer-reviewed open access monthly 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 2600 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

  • preterm birth
  • placenta
  • fetal membranes
  • feto–maternal interface
  • chorioamnionitis
  • ascending intrauterine infection
  • fetal vascular malperfusion
  • maternal vascular malperfusion
  • neonatal morbidity
  • preterm labor
  • preterm-PROM
  • preeclampsia
  • fetal growth restriction

Published Papers (1 paper)

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Research

14 pages, 1439 KiB  
Article
Examining the Aryl Hydrocarbon Receptor Network in the Placental Tissues of Pregnancies Complicated by Pre-Eclampsia: An Explorative Case–Control Analysis
by Serena Xodo, Ambrogio P. Londero, Maria Orsaria, Stefania Marzinotto, Gianluca Colussi, Angelo Cagnacci, Laura Mariuzzi and Giorgia Gri
Life 2023, 13(11), 2122; https://doi.org/10.3390/life13112122 - 26 Oct 2023
Viewed by 789
Abstract
Severe maternal and newborn morbidity and mortality associated with pre-eclampsia, which are caused partly by premature delivery, affect a factual proportion of pregnancies. Despite its prevalence, the underlying causes of pre-eclampsia remain elusive, with emerging evidence implicating the aryl hydrocarbon receptor (AhR) in [...] Read more.
Severe maternal and newborn morbidity and mortality associated with pre-eclampsia, which are caused partly by premature delivery, affect a factual proportion of pregnancies. Despite its prevalence, the underlying causes of pre-eclampsia remain elusive, with emerging evidence implicating the aryl hydrocarbon receptor (AhR) in its pathogenesis. This study sought to elucidate the involvement of the AhR and its associated pathway in pre-eclampsia by comparing placental components of the AhR pathway in pregnant individuals with and without pre-eclampsia. This case–control investigation was conducted at the University Hospital of Udine from May 2021 to February 2023. The AhR was assessed using immunohistochemistry and immunofluorescence, and its mRNA was evaluated using a Real-Time Quantitative Reverse Transcription PCR. Levels of mRNA expression were also estimated for other components of the AhR pathway (CYP1B1, IDO1, ARNT, TIPARP, S100A4, and AHRR). Our findings show decreased levels of expression of AhR, IDO1, ARNT, TiPARP, and S100A4 in the placental tissues of individuals with pre-eclampsia compared to controls (p < 0.05). The AhR exhibited a distinct localization within the syncytiotrophoblast (nuclei and cytoplasm) and CD45-positive cells (nuclei and cytoplasm). Furthermore, a significant positive correlation between the AhR and S100A4 (rho = 0.81) was observed in normal placentas, while CYP1B1 displayed a significant negative correlation with the AhR (rho = −0.72), within addition to its negative correlation with TiPARP (rho = −0.83). This study illuminates pre-eclampsia’s molecular aberrations, suggesting new diagnostic, therapeutic, and mechanistic approaches. This study emphasizes the need for more research to validate and broaden these findings to improve the management of this complex pregnancy condition. Full article
(This article belongs to the Special Issue New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth Version 2.0)
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