The Placental Matrix: Trophoblasts, Decidualization, and Embryo Implantation

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

Deadline for manuscript submissions: 20 September 2025 | Viewed by 178

Special Issue Editor


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Guest Editor
Department of Obstetrics, Gynecology and Reproductive Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
Interests: placenta; trophoblast; decidualization; embryo implantation

Special Issue Information

Dear Colleagues,

The placenta is essential for pregnancy success, orchestrating a complex interplay between trophoblast differentiation, decidualization, and immune modulation to ensure proper embryo implantation and maternal–fetal communication. Disruptions in these tightly regulated processes, especially due to inflammation and environmental toxicants, can trigger severe pregnancy complications, including implantation failure, pre-eclampsia, fetal growth restriction, and long-term offspring health consequences. Deciphering the molecular and cellular mechanisms underlying these interactions is critical for developing targeted interventions to improve reproductive outcomes. This Special Issue delves into the latest advancements in placental biology, immune crosstalk, and reproductive toxicology, shedding light on how environmental and inflammatory factors shape pregnancy health.

Dr. Vinay Shukla
Guest Editor

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Keywords

  • trophoblast
  • decidualization
  • embryo implantation
  • uterus
  • infection
  • cancer
  • reproductive immunology
  • reproductive toxicology
  • cellular differentiation

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Published Papers (1 paper)

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Research

20 pages, 1436 KB  
Article
Maternal Exposure to Diesel Exhaust Particles (DEPs) During Pregnancy and Adverse Pregnancy Outcomes: Focusing on the Effect of Particulate Matter on Trophoblast, Epithelial-Mesenchymal Transition
by Hyewon Hur, Hayan Kwon, Yun Ji Jung, Euna Choi, Joonggyeong Shin, Subin Jo, Yeji Lee, Min-A Kim, Yong-Sun Maeng and Ja-Young Kwon
Cells 2025, 14(17), 1317; https://doi.org/10.3390/cells14171317 - 26 Aug 2025
Abstract
During pregnancy, exposure to fine particulate matter (PM2.5), particularly diesel exhaust particles (DEPs), elevates the risk of placental dysfunction-related pregnancy complications; however, the underlying cellular mechanisms have yet to be fully elucidated. The objective of this study was to assess the [...] Read more.
During pregnancy, exposure to fine particulate matter (PM2.5), particularly diesel exhaust particles (DEPs), elevates the risk of placental dysfunction-related pregnancy complications; however, the underlying cellular mechanisms have yet to be fully elucidated. The objective of this study was to assess the effects of PM2.5 exposure on trophoblast functions and their interaction with endometrial stromal cells. We utilized a three-dimensional (3D) model in which human first-trimester trophoblasts (Sw71) formed blastocyst-like spheroids and were cultured with human endometrial stromal cells (HESCs). Trophoblast proliferation, migration, invasion, and 3D network formation following DEP exposure (0.5–20 μg/mL) were assessed using methyl thiazolyl diphenyl-tetrazolium bromide (MTT), wound healing, migration, and invasion assays. The expression levels of genes related to the epithelial-mesenchymal transition (EMT) were quantified by real-time reverse-transcription quantitative polymerase chain reaction (RT-qPCR). DEP exposure significantly inhibited trophoblast proliferation, migration, and invasion. DEP treatment dysregulated the EMT program by significantly decreasing the expression of key mesenchymal markers (SNAI1, SNAI2, SOX2, and KLF4) while upregulating epithelial markers. These changes may be related to inhibited trophoblast migration toward HESC monolayers and 3D invasive network formation. DEP directly impairs critical trophoblast functions that are essential for successful pregnancy. Disruption of the EMT program represents a molecular mechanism by which traffic-related air pollution contributes to placental dysfunction and pregnancy complications, highlighting the significant reproductive risks posed by ambient air pollution. Full article
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