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Biology
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Development and Pathophysiology of the Placenta
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Development and Pathophysiology of the Placenta

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Reproductive Biology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3258

Special Issue Editors

Dr. Mary C. Wallingford

E-Mail Website
Guest Editor
Mother Infant Research Institute, Tufts Medical Center, Boston, MA 02111, USA
Interests: cardiovascular biology; developmental biology; placenta; pregnancy; vascular biology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kun Zhang

E-Mail Website
Guest Editor
College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
Interests: preimplantation; embryo; epigenetics; genome editing; cattle; pig; mouse
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The methods and techniques available to support placenta research have expanded significantly over the last decade, shedding unprecedent insight into placental development and pathophysiology. For example, high throughput omics studies expand our molecular knowledge regarding placental factors, from genetic variants, to diverse RNA spliceforms, to stage-specific placental proteomes and epigenomes. Along another vein, advanced imaging modalities and improved imaging approaches and image analysis techniques are rapidly improving noninvasive assessment of placental size, shape, and physiology. The continued integration of animal models of disease with pregnancy research has also greatly advanced knowledge of numerous parameters that can influence placental development and physiology and, in turn, maternal and fetal outcomes. Finally, the technical advancements of microfluidic devices, organ-on-a-chip in vitro models, iPSC methods, and organoid protocols have provided a flourish of tractable systems that investigators have begun to use to study transplacental transport and functionality of discrete aspects of the placenta.

Overall, there is an emerging consensus in the field regarding the significance of temporal changes in the placenta. Indeed, the placenta is a complex organ that rapidly develops, remodels, and eventually transitions into a dynamic aging program as pregnancy advances.

This Special Issue specifically invites original research papers and reviews that capture the dynamic nature of placental development and pathophysiology. We welcome studies involving computational, cell and tissue culture, animal model, and translational and clinical research approaches that advance knowledge of developmental mechanisms and functional assessments of the placenta across all stages of pregnancy, from implantation to parturition.

Dr. Mary C. Wallingford
Prof. Dr. Kun Zhang
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. Biology 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 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.

Keywords

  • endothelial cells
  • implantation
  • maternal-fetal interface
  • placenta
  • placentation
  • trophoblast, trophectoderm

Published Papers (2 papers)

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Research

14 pages, 2225 KiB  
Article
Detection of Math6-Expressing Cell Types in Murine Placenta
by Maren Brendel, Marion Scharf, Urs Kindler, Satya Srirama Karthik Divvela and Beate Brand-Saberi
Biology 2023, 12(9), 1252; https://doi.org/10.3390/biology12091252 - 19 Sep 2023
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Abstract
The transcription factor Math6, mouse atonal homolog 6, belongs to the family of highly conserved basic helix–loop–helix transcription factors. It plays an important role in embryonic development and shows a wide expression pattern in murine tissues. The placenta, as a life-sustaining transient organ [...] Read more.
The transcription factor Math6, mouse atonal homolog 6, belongs to the family of highly conserved basic helix–loop–helix transcription factors. It plays an important role in embryonic development and shows a wide expression pattern in murine tissues. The placenta, as a life-sustaining transient organ for the fetus, also depends on the expression of Math6. The adverse effects of deleting Math6 in mice, leading to deficient placental development and pregnancy loss, have already been demonstrated by us. Until now, detailed investigations regarding the specific mechanisms underlying the improper placental development in these murine mutants have failed, as the Math6 expression could not be confined to a specific cell type due to the lack of a highly specific Math6 antibody. To circumvent this problem, we used transgenic mice, where Math6 is marked with a Flag sequence that functions as a specific epitope. Tissues from these transgenic mice were used to establish immunohistochemical staining and fluorescence-activated cell sorting (FACS). The establishment of these methods yielded initial findings pertaining to the identification of Math6-expressing cell types and their localization. Our results reveal that Math6 shows a wide expression pattern in both maternal and fetal components of the murine placenta. It shows expression in various cell types, but predominantly in trophoblast giant cells, endothelial cells and macrophages. The largest subpopulation that we detected in the group of Math6-positive cells were identified as DBA+ uterine natural killer cells. These findings reveal information and a chance for further investigation on the involvement of Math6 in placental development and the molecular pathomechanisms of spontaneous abortion. Full article
(This article belongs to the Special Issue Development and Pathophysiology of the Placenta)
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12 pages, 1414 KiB  
Article
Lipid Aldehydes 4-Hydroxynonenal and 4-Hydroxyhexenal Exposure Differentially Impact Lipogenic Pathways in Human Placenta
by Aisha Rasool, Taysir Mahmoud and Perrie O’Tierney-Ginn
Biology 2023, 12(4), 527; https://doi.org/10.3390/biology12040527 - 30 Mar 2023
Cited by 1 | Viewed by 1694
Abstract
Long chain polyunsaturated fatty acids (LCPUFAs), such as the omega-6 (n-6) arachidonic acid (AA) and n-3 docosahexanoic acid (DHA), have a vital role in normal fetal development and placental function. Optimal supply of these LCPUFAs to the fetus is critical for improving birth [...] Read more.
Long chain polyunsaturated fatty acids (LCPUFAs), such as the omega-6 (n-6) arachidonic acid (AA) and n-3 docosahexanoic acid (DHA), have a vital role in normal fetal development and placental function. Optimal supply of these LCPUFAs to the fetus is critical for improving birth outcomes and preventing programming of metabolic diseases in later life. Although not explicitly required/recommended, many pregnant women take n-3 LCPUFA supplements. Oxidative stress can cause these LCPUFAs to undergo lipid peroxidation, creating toxic compounds called lipid aldehydes. These by-products can lead to an inflammatory state and negatively impact tissue function, though little is known about their effects on the placenta. Placental exposure to two major lipid aldehydes, 4-hydroxynonenal (4-HNE) and 4-hydroxyhexenal (4-HHE), caused by peroxidation of the AA and DHA, respectively, was examined in the context of lipid metabolism. We assessed the impact of exposure to 25 μM, 50 μM and 100 μM of 4-HNE or 4-HHE on 40 lipid metabolism genes in full-term human placenta. 4-HNE increased gene expression associated with lipogenesis and lipid uptake (ACC, FASN, ACAT1, FATP4), and 4-HHE decreased gene expression associated with lipogenesis and lipid uptake (SREBP1, SREBP2, LDLR, SCD1, MFSD2a). These results demonstrate that these lipid aldehydes differentially affect expression of placental FA metabolism genes in the human placenta and may have implications for the impact of LCPUFA supplementation in environments of oxidative stress. Full article
(This article belongs to the Special Issue Development and Pathophysiology of the Placenta)
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