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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

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 December 2021) | Viewed by 9408

Special Issue Editors

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
Prof. Dr. Ramkumar Menon

E-Mail Website
Guest Editor
Department of Obstetrics & Gynecology, Division of Maternal-Fetal Medicine Perinatal Research, The University of Texas Medical Branch at Galveston, 301 University Blvd., Galveston, TX 77555, USA
Interests: fetal tissue senescence and senescence associated cellular transitions in reproductive tissues; extracellular vesicle mediated signaling between feto-maternal tissues; development of organ-on-chip technology for intrauterine tissues; engineering and testing of extracellular vesicles as drug delivery vehicles; use of organ-on-chip in preclinical drug trials; development and testing of extracellular vesicle based drugs for reduction of preterm birth

Special Issue Information

Dear Colleagues,

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

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

Dr. Chan-wook Park
Prof. Dr. Ramkumar Menon
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. 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 (4 papers)

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14 pages, 4377 KiB  
Article
Preterm Labor and Preterm-PROM at a Lower Gestational Age Are Associated with a Longer Latency-to-Delivery Even in Patients with the Same Intensity of Intra-Amniotic Inflammation: “Carroll-Model” Revisited
by Jeong-Won Sohn, Eun-Saem Choi, Chan-Wook Park, Kyung-Chul Moon, Joong-Shin Park and Jong-Kwan Jun
Life 2022, 12(9), 1329; https://doi.org/10.3390/life12091329 - 27 Aug 2022
Viewed by 1570
Abstract
A previous study by Carroll et al. demonstrated that the time from preterm-PROM to delivery was longer at a lower gestational age (GA) when the membranes rupture, although the presence or absence of intra-amniotic inflammation (IAI) was not examined in that study. However, [...] Read more.
A previous study by Carroll et al. demonstrated that the time from preterm-PROM to delivery was longer at a lower gestational age (GA) when the membranes rupture, although the presence or absence of intra-amniotic inflammation (IAI) was not examined in that study. However, patients with either preterm labor (PTL) or preterm-PROM at a lower GA had more frequent IAI, which was associated with a shorter amniocentesis-to-delivery (ATD) interval as compared with inflammation-free amniotic fluid (AF). Up to now, there is no information about whether PTL and preterm-PROM at a lower GA are associated with a shorter or longer latency to delivery in cases with the same intensity of IAI. The objective of the study is to examine this issue. AF MMP-8 was measured in 476 singleton early preterm-gestations (21.5 < GA at amniocentesis < 34 wks) with PTL (n = 253) and preterm-PROM (n = 223). Patients were divided into three groups according to GA at amniocentesis (i.e., group-1: <26 wks; group-2: 26–30 wks; group-3: 30–34 wks). IAI was defined as an elevated AF MMP-8 (≥23 ng/mL), and IAI was classified into either mild IAI (AF MMP-8: 23–350 ng/mL) or severe IAI (AF MMP-8 ≥ 350 ng/mL). ATD interval was examined according to GA at amniocentesis in the context of the same intensity of IAI (i.e., inflammation-free AF, mild IAI, and severe IAI) among pregnant women with either PTL or preterm-PROM. IAI was more frequent at a lower GA in cases with PTL (group-1 vs. group-2 vs. group-3; 59.5% vs. 47.4% vs. 25.1%; X2test, p = 0.000034 and linear by linear association [LBLA], p = 0.000008) and in those with preterm-PROM (group-1 vs. group-2 vs. group-3; 69.2% vs. 50.0% vs. 32.0%; X2test, p = 0.000104, and LBLA, p = 0.000019). Of note, cases without IAI at a lower GA had a longer ATD interval in both PTL (Spearman’s rank correlation test, γ = −0.360, p = 0.000003) and preterm-PROM (γ = −0.570, p = 0.000001) groups. Moreover, the lower the GA, the longer the ATD interval, even among patients with mild and severe IAI in both PTL (Spearman’s rank correlation test; mild IAI, γ = −0.290, p = 0.039; severe IAI, γ = −0.299, p = 0.048) and preterm-PROM (mild IAI, γ = −0.565, p = 0.000013; severe IAI, γ = −0.363, p = 0.015) groups. In conclusion, PTL and preterm-PROM at a lower GA are associated with a longer latency to delivery, even in patients with the same intensity of IAI. This finding suggests that a more intense IAI may be needed for spontaneous preterm birth at a lower GA. Full article
(This article belongs to the Special Issue New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth)
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16 pages, 4202 KiB  
Article
Dysregulation of the Amniotic PPARγ Pathway by Phthalates: Modulation of the Anti-Inflammatory Activity of PPARγ in Human Fetal Membranes
by Audrey Antoine, Coraline De Sousa Do Outeiro, Coline Charnay, Corinne Belville, Fanny Henrioux, Denis Gallot, Loïc Blanchon, Régine Minet-Quinard and Vincent Sapin
Life 2022, 12(4), 544; https://doi.org/10.3390/life12040544 - 06 Apr 2022
Cited by 1 | Viewed by 1670
Abstract
Phthalates are reprotoxic pollutants that are omnipresent in the environment. Detectable in amniotic fluid, these compounds (with the most concentrated being mono-2-ethylhexyl phthalate (MEHP)) are in direct contact with fetal membranes (FMs). They can lead to the premature rupture of FMs by deregulating [...] Read more.
Phthalates are reprotoxic pollutants that are omnipresent in the environment. Detectable in amniotic fluid, these compounds (with the most concentrated being mono-2-ethylhexyl phthalate (MEHP)) are in direct contact with fetal membranes (FMs). They can lead to the premature rupture of FMs by deregulating cellular and molecular pathways, such as, for example, the nuclear transcription factor peroxysome proliferator-activated receptor gamma (PPARγ) pathway. The objective was to study the impact of MEHP on the PPARγ pathway in FMs using amnion and choriodecidua across the three trimesters of pregnancy and the amniotic epithelial AV3 cell model by analyzing (i) PPARγ expression (mRNA and proteins) using RT-qPCR and Western blot assays; (ii) cytotoxicity and cell viability following MEHP treatment by lactate dehydrogenase (LDH) measurement and using Cell-counting Kit 8; and (iii) modulation by MEHP of PPARγ transcriptional activity (using a reporter gene assay) and PPARγ anti-inflammatory properties (by measuring IL6 and IL8 levels). PPARγ is expressed in the human amnion and choriodecidua during the three trimesters of pregnancy and in amniotic cells. In the AV3 cell line, MEHP is not cytotoxic and does not reduce cell viability, but it reduces PPARγ activity, here induced by a classical agonist without influencing its expression. MEHP also reduces PPARγ’s anti-inflammatory properties. In conclusion, PPARγ signaling is dysregulated by MEHP; this paves the way for future explorations to highlight the hypothesis of phthalates as an amniotic PPARγ disruptor that can explain the premature rupture of FMs. Full article
(This article belongs to the Special Issue New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth)
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14 pages, 2052 KiB  
Article
Fetal Membranes Contribute to Drug Transport across the Feto-Maternal Interface Utilizing the Breast Cancer Resistance Protein (BCRP)
by Ananthkumar Kammala, Meagan Benson, Esha Ganguly, Enkhtuya Radnaa, Talar Kechichian, Lauren Richardson and Ramkumar Menon
Life 2022, 12(2), 166; https://doi.org/10.3390/life12020166 - 23 Jan 2022
Cited by 11 | Viewed by 2936
Abstract
During pregnancy, the placenta is established as a primary organ for drug transport at the maternal-fetal interface. The fetal membranes (FM) also form an interface with maternal tissues; however, their role in drug transport has not been previously investigated. Knowledge of drug transport [...] Read more.
During pregnancy, the placenta is established as a primary organ for drug transport at the maternal-fetal interface. The fetal membranes (FM) also form an interface with maternal tissues; however, their role in drug transport has not been previously investigated. Knowledge of drug transport across this feto-maternal interface along with the placenta can improve new drug development and testing for use during pregnancy. We also hypothesize that extracellular vesicles (exosomes 30–160 nm) released from the FM and placental cells may also contain drug transport proteins and might impact drug trafficking across the feto-maternal interfaces. The objectives were to (1) localize the breast cancer resistance protein (BCRP) in human FM; (2) determine the drug transport function of BCRP in chorion trophoblast cells (CTCs) of the FM; and (3) investigate the presence of BCRP in FM cell-derived exosomes, as a paracrine modifier of the tissue environment for transport functions. The gene and protein expressions of ABCG2/BCRP in FMs were determined by quantitative real-time PCR (qRT-PCR) and western blotting (WB) and were localized by immunohistochemistry (IHC). The surface expression of BCRP in FM cells was determined by flow cytometry. The functional role of BCRP was assessed by an EFFLUX dye multidrug resistance assay. The presence of BCRP in exosomes derived from CTCs and BeWo cells was examined using ExoView®. Data derived from CTCs are compared with placental trophoblast cells (BeWo). BCRP is expressed and localized in the fetal membrane, primarily in the chorion trophoblast cell layer and scarcely in the amnion epithelial layer (AEC), and primarily localized on both AEC and CTC cell surfaces. Efflux assay data showed that FM cells have similar drug resistance activity as BeWo cells, suggesting that FM also have drug transportation capabilities. BeWo- and CTC-derived exosomes expressed limited BCRP protein on the surface, so it was predominantly contained in the exosomal lumen. As far as we are aware, this is the first study to report BCRP expression in fetal membrane cells and as cargo in fetal membrane-derived exosomes. We report that fetal membrane cells are capable of drug transportation. Based on these results, investigational drug trials should include the FM and its exosomes as possible drug transportation routes in pregnancy. Full article
(This article belongs to the Special Issue New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth)
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14 pages, 2254 KiB  
Systematic Review
Histocompatibility Antigen, Class I, G (HLA-G)’s Role during Pregnancy and Parturition: A Systematic Review of the Literature
by Ourlad Alzeus G. Tantengco, Lauren Richardson, Alan Lee, Ananthkumar Kammala, Mariana de Castro Silva, Hend Shahin, Samantha Sheller-Miller and Ramkumar Menon
Life 2021, 11(10), 1061; https://doi.org/10.3390/life11101061 - 09 Oct 2021
Cited by 8 | Viewed by 2109
Abstract
Introduction: Immune homeostasis of the intrauterine cavity is vital for pregnancy maintenance. At term or preterm, fetal and maternal tissue inflammation contributes to the onset of labor. Though multiple immune-modulating molecules are known, human leukocyte antigen (HLA)-G is unique to gestational tissues and [...] Read more.
Introduction: Immune homeostasis of the intrauterine cavity is vital for pregnancy maintenance. At term or preterm, fetal and maternal tissue inflammation contributes to the onset of labor. Though multiple immune-modulating molecules are known, human leukocyte antigen (HLA)-G is unique to gestational tissues and contributes to maternal–fetal immune tolerance. Several reports on HLA-G’s role exist; however, ambiguity exists regarding its functional contributions during pregnancy and parturition. To fill these knowledge gaps, a systematic review (SR) of the literature was conducted to better understand the expression, localization, function, and regulation of HLA-G during pregnancy and parturition. Methods: A SR of the literature on HLA-G expression and function reported in reproductive tissues during pregnancy, published between 1976–2020 in English, using three electronic databases (SCOPE, Medline, and ClinicalTrials.gov) was conducted. The selection of studies, data extraction, and quality assessment were performed in duplicate by two independent reviewers. Manuscripts were separated into three categories: (1) expression and localization of HLA-G, (2) regulators of HLA-G, and (3) the mechanistic roles of HAL-G. Data were extracted, analyzed, and summarized. Results: The literature search yielded 2554 citations, 117 of which were selected for full-text evaluation, and 115 were included for the final review based on our inclusion/exclusion criteria. HLA-G expression and function were mostly studied in placental tissue and/or cells and peripheral blood immune cells, while only 13% of the studies reported data on amniotic fluid/cord blood and fetal membranes. Measurements of soluble and membranous HLA-G were determined mostly by RNA-based methods and protein by immunostaining, Western blot, or flow cytometric analyses. HLA-G was reported to regulate inflammation and inhibit immune-cell-mediated cytotoxicity and trophoblast invasion. Clinically, downregulation of HLA-G is reported to be associated with poor placentation in preeclampsia and immune cell infiltration during ascending infection. Conclusions: This SR identified several reports supporting the hypothesized role of immune regulation in gestational tissues during pregnancy. A lack of rigor and reproducibility in the experimental approaches and models in several reports make it difficult to fully elucidate the mechanisms of action of HLA-G in immune tolerance during pregnancy. Full article
(This article belongs to the Special Issue New Insights into the Placental and Placental Membrane Pathophysiology of Preterm Birth)
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