Human Placenta and Trophoblast Cells in Pregnancy Development

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

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 4175

Special Issue Editor


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Guest Editor
Department of Cell Biology and Physiology, Brigham Young University, Provo, UT, USA
Interests: placental development; trophoblast functioning; obstetric complications

Special Issue Information

Dear Colleagues,

Maternal–fetal interactions mediated by the placenta are critical to fetal development and overall positive outcomes during pregnancy. During gestation, the placenta mediates the interface between mother and fetus, regulating processes such as gas exchange, nutrition availability, and waste removal. The first differentiation event during placental development is the formation of trophoblast—specialized epithelial cells that form a physical connection between the embryo and the uterus. Aberrant trophoblast functioning is associated with placental deficiencies and clinical obstetric pathologies.

This Special Issue will examine the direct correlation between placenta and their trophoblast cells functioning in the development of normal and complicated pregnancies.

Dr. Juan Arroyo
Guest Editor

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Keywords

  • placenta
  • trophoblast
  • pregnancy

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Published Papers (3 papers)

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Research

23 pages, 15987 KiB  
Article
Small and Long Non-Coding RNA Analysis for Human Trophoblast-Derived Extracellular Vesicles and Their Effect on the Transcriptome Profile of Human Neural Progenitor Cells
by Jessica A. Kinkade, Pallav Singh, Mohit Verma, Teka Khan, Toshihiko Ezashi, Nathan J. Bivens, R. Michael Roberts, Trupti Joshi and Cheryl S. Rosenfeld
Cells 2024, 13(22), 1867; https://doi.org/10.3390/cells13221867 - 11 Nov 2024
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Abstract
In mice, the fetal brain is dependent upon the placenta for factors that guide its early development. This linkage between the two organs has given rise to the term, the placenta–brain axis. A similar interrelationship between the two organs may exist in humans. [...] Read more.
In mice, the fetal brain is dependent upon the placenta for factors that guide its early development. This linkage between the two organs has given rise to the term, the placenta–brain axis. A similar interrelationship between the two organs may exist in humans. We hypothesize that extracellular vesicles (EVs) released from placental trophoblast (TB) cells transport small RNA and other informational biomolecules from the placenta to the brain where their contents have pleiotropic effects. Here, EVs were isolated from the medium in which human trophoblasts (TBs) had been differentiated in vitro from induced pluripotent stem cells (iPSC) and from cultured iPSC themselves, and their small RNA content analyzed by bulk RNA-seq. EVs derived from human TB cells possess unique profiles of miRs, including hsa-miR-0149-3p, hsa-302a-5p, and many long non-coding RNAs (lncRNAs) relative to EVs isolated from parental iPSC. These miRs and their mRNA targets are enriched in neural tissue. Human neural progenitor cells (NPCs), generated from the same iPSC, were exposed to EVs from either TB or iPSC controls. Both sets of EVs were readily internalized. EVs from TB cells upregulate several transcripts in NPCs associated with forebrain formation and neurogenesis; those from control iPSC upregulated a transcriptional phenotype that resembled glial cells more closely than neurons. These results shed light on the possible workings of the placenta–brain axis. Understanding how the contents of small RNA within TB-derived EVs affect NPCs might yield new insights, possible biomarkers, and potential treatment strategies for neurobehavioral disorders that originate in utero, such as autism spectrum disorders (ASDs). Full article
(This article belongs to the Special Issue Human Placenta and Trophoblast Cells in Pregnancy Development)
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19 pages, 3162 KiB  
Article
Different Lengths of Gestational Exposure to Secondhand Smoke or e-Cigarette Vapor Induce the Development of Placental Disease Symptoms
by Madison N. Kirkham, Christian Cooper, Emily Broberg, Peter Robertson, Derek Clarke, Brett E. Pickett, Benjamin Bikman, Paul R. Reynolds and Juan A. Arroyo
Cells 2024, 13(12), 1009; https://doi.org/10.3390/cells13121009 - 9 Jun 2024
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Abstract
Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has [...] Read more.
Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has recently emerged, and their use is also steadily rising. Even so, the effects of SHS or eCigs during gestation remain limited. In the present study, we wanted to characterize the effects of SHS or eCig exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS or eCigs via a nose-only delivery system for 4 days (from 14.5 to 17.5 gestational days (dGA) or for 6 days (from 12.5 dGA to 17.5 dGA)). At the time of necropsy (18.5 dGA), placental and fetal weights were recorded, maternal blood pressure was determined, and a dipstick test to measure proteinuria was performed. Placental tissues were collected, and inflammatory molecules in the placenta were identified. Treatment with SHS showed the following: (1) a significant decrease in placental and fetal weights following four days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. Treatment with eCigs showed the following: (1) a significant decrease in placental weight and fetal weight following four or six days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. We also observed different inflammatory markers associated with the development of IUGR or PE. We conclude that the detrimental effects of SHS or eCig treatment coincide with the length of maternal exposure. These results could be beneficial in understanding the long-term effects of SHS or eCig exposure in the development of placental diseases. Full article
(This article belongs to the Special Issue Human Placenta and Trophoblast Cells in Pregnancy Development)
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12 pages, 1823 KiB  
Article
An Examination of the Effect of Aspirin and Salicylic Acid on Soluble Fms-like Tyrosine Kinase-1 Release from Human Placental Trophoblasts
by Jiawu Zhao, Rui Duan, Jinghui Sun, Rebecca P. Chow, Timothy J. Lyons and Jeremy Y. Yu
Cells 2024, 13(2), 113; https://doi.org/10.3390/cells13020113 - 6 Jan 2024
Cited by 1 | Viewed by 1595
Abstract
Low-dose aspirin (LDA) is efficacious in preventing preeclampsia, but its mechanism of action is unclear. Conflicting evidence suggests that it may inhibit placental trophoblast release of soluble fms-like tyrosine kinase-1 (sFlt1), a key mediator of preeclampsia. We examined whether, and at what concentrations, [...] Read more.
Low-dose aspirin (LDA) is efficacious in preventing preeclampsia, but its mechanism of action is unclear. Conflicting evidence suggests that it may inhibit placental trophoblast release of soluble fms-like tyrosine kinase-1 (sFlt1), a key mediator of preeclampsia. We examined whether, and at what concentrations, aspirin and its principal metabolite, salicylic acid, modulate sFlt1 release and/or expression in trophoblasts. Human trophoblast lines BeWo and HTR-8/SVneo were cultured; BeWo cells were also treated with 1% oxygen vs. normoxia to mimic hypoxia in preeclamptic placentas. Cells were treated with aspirin or salicylic acid vs. vehicle for 24 h at concentrations relevant to LDA and at higher concentrations. Protein concentrations (ELISA) and mRNA expression (RT-PCR) of sFlt1 were determined. Under normoxia, LDA-relevant concentrations of aspirin (10–50 µmol/L) or salicylic acid (20–100 µmol/L) had no significant effect on sFlt1 protein release or mRNA expression in BeWo cells. However, inhibition was observed at higher concentrations (1 mmol/L for aspirin and ≥200 μmol/L for salicylic acid). Hypoxia enhanced sFlt1 protein release and mRNA expression in BeWo cells, but these responses were not significantly affected by either aspirin or salicylic acid at LDA concentrations. Similarly, neither drug altered sFlt1 protein secretion or mRNA expression in normoxic HTR-8/SVneo cells at LDA concentrations. We suggest that direct modulation of trophoblast release or expression of sFlt1 is unlikely to be a mechanism underlying the clinical efficacy of LDA in preeclampsia. Full article
(This article belongs to the Special Issue Human Placenta and Trophoblast Cells in Pregnancy Development)
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