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Biomolecules
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Placental-Related Disorders of Pregnancy: 2nd Edition
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Placental-Related Disorders of Pregnancy: 2nd Edition

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 15 February 2025 | Viewed by 7746

Special Issue Editor

Dr. Zaneta Kimber-Trojnar

E-Mail Website
Guest Editor
Chair and Department of Obstetrics and Perinatology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: gestational diabetes mellitus; fetal growth restriction; preeclampsia biomarkers; preterm delivery; fetal programming; excessive gestational weight gain; metabolic syndrome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a very successful first run, we are pleased to announce the launch of a second edition of a Special Issue entitled “Placental-Related Disorders of Pregnancy”.

The placenta is a unique, multifunctional organ that develops exclusively in pregnancy and results from complex interactions between the tissues of the fetus and the mother. It is responsible for exchanging nutrients, gases and wastes between the maternal and fetal circulations. The placenta is also an important endocrine organ that produces hormones indispensable to supporting pregnancy and regulating feto-maternal physiology. The main function of the placenta, however, is to maintain the environmental homeostasis required for fetal growth.

Placental-related disorders, which affect about a third of human pregnancies, manifest via different symptoms diseases and complications. Examples of these illnesses include preeclampsia, intrauterine growth restriction, placental abruption and placenta accreta, all of which contribute to increased maternal and perinatal morbidity and mortality. Placental dysfunction and programming may also have lifelong health consequences for both mother and offspring. Delayed reproductive plans, the incidence of cesarean sections, and lifestyle changes, including improper diet, appear to have increased the incidence of placental-related disorders and diseases in recent decades.

We invite the scientific community to submit original articles and reviews on placentation and placental-related disorders to provide some novel insight into any aspect of placental biochemistry. We believe that, with your input, this Special Issue will shed more light on the mechanisms involved in the development of placental pathologies and help to find biomolecules for their prediction and early diagnosis.

Dr. Zaneta Kimber-Trojnar
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. Biomolecules 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

  • placenta
  • preeclampsia
  • intrauterine growth restriction
  • placental abruption
  • placenta accrete
  • biomolecules
  • fetal programming
  • maternal programming
  • endothelial dysfunction
  • inflammation
  • oxidative stress

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Related Special Issue

Published Papers (3 papers)

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Research

14 pages, 1930 KiB  
Article
The Significance of Selected Collagens and Their Connection with Relevant Extracellular Matrix Proteins in Bovine Early-Mid-Pregnancy and Parturition with and Without Retained Foetal Membranes
by Jacek Wawrzykowski, Monika Jamioł and Marta Kankofer
Biomolecules 2025, 15(2), 167; https://doi.org/10.3390/biom15020167 - 23 Jan 2025
Viewed by 428
Abstract
Appropriate placental structure and function assure foetal development, delivery of nutrients, and removal of waste. Collagens, as structural proteins, are crucial for the maintenance of placental growth and function. The aim of this study was to describe the profile of collagen 1 and [...] Read more.
Appropriate placental structure and function assure foetal development, delivery of nutrients, and removal of waste. Collagens, as structural proteins, are crucial for the maintenance of placental growth and function. The aim of this study was to describe the profile of collagen 1 and 4 in the placental tissues of cows and to correlate it to previously described activities of collagenases and adhesive proteins. Placental samples were collected from pregnant cows in the slaughterhouse (2nd, 4th, and 6th month; n = 12) and during parturition after caesarean section. Samples taken during caesarean section were retrospectively divided into retained (R; n = 6) and not retained foetal membranes (NR; n = 6). Determinations were performed of maternal and foetal parts separately after tissue homogenisation. Supernatants were used for the determination of COL1 and COL4 concentrations by ELISA and WB analysis. Significant differences were detected between pregnancy months and parturient samples in COL1 concentrations and between retained and released foetal membranes. The concentrations of COL4 were higher in the foetal as compared to the maternal part of the placenta. Significant differences were detected between retained and released foetal membranes, and, similarly to Col1, values were lower in retained than released foetal membranes. WB analysis showed the presence of examined collagen molecules and their molecular weights. The analysis of collagen profile together with the enzymes of their degradation and other adhesive proteins (glycodelin, decorin, and thrombospondins) in bovine placenta either during pregnancy and parturition showed a close relationship. Either attachment or detachment of the maternal and foetal parts of the bovine placenta requires actions in concert between all these adhesive proteins under the influence of pregnancy hormones. Full article
(This article belongs to the Special Issue Placental-Related Disorders of Pregnancy: 2nd Edition)
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21 pages, 8909 KiB  
Article
The Role of MALAT1 in Regulating the Proangiogenic Functions, Invasion, and Migration of Trophoblasts in Selective Fetal Growth Restriction
by Shuting Xia, Yingnan Ye, Jialiu Liu, Hanfei Qiu, Minhuan Lin, Zhiming He, Linhuan Huang, Malie Wang and Yanmin Luo
Biomolecules 2024, 14(8), 988; https://doi.org/10.3390/biom14080988 - 11 Aug 2024
Cited by 1 | Viewed by 3932
Abstract
Epigenetic regulation is an important entry point to study the pathogenesis of selective fetal growth restriction (sFGR), and an understanding of the role of long noncoding RNAs (lncRNAs) in sFGR is lacking. Our study aimed to investigate the potential role of a lncRNA, [...] Read more.
Epigenetic regulation is an important entry point to study the pathogenesis of selective fetal growth restriction (sFGR), and an understanding of the role of long noncoding RNAs (lncRNAs) in sFGR is lacking. Our study aimed to investigate the potential role of a lncRNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), in sFGR using molecular biology experiments and gain- or loss-of-function assays. We found that the levels of MALAT1, ERRγ, and HSD17B1 were downregulated and that of miR-424 was upregulated in the placental shares of the smaller twins. Moreover, angiogenesis was impaired in the placental share of the smaller fetus and MALAT1 could regulate the paracrine effects of trophoblasts on endothelium angiogenesis and proliferation by regulating miR-424. In trophoblasts, MALAT1 could competitively bind to miR-424 to regulate the expression of ERRγ and HSD17B1, thus regulating trophoblast invasion and migration. MALAT1 overexpression could decrease apoptosis and promote proliferation, alleviating cell damage induced by hypoxia. Taken together, the downregulation of MALAT1 can reduce the expression of ERRγ and HSD17B1 by competitively binding to miR-424, impairing the proangiogenic effect of trophoblasts, trophoblast invasion and migration, and the ability of trophoblasts to compensate for hypoxia, which may be involved in the pathogenesis of sFGR through various aspects. Full article
(This article belongs to the Special Issue Placental-Related Disorders of Pregnancy: 2nd Edition)
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17 pages, 21708 KiB  
Article
High Glucose Promotes and Aggravates the Senescence and Dysfunction of Vascular Endothelial Cells in Women with Hyperglycemia in Pregnancy
by Lin Zheng, Mingqing Li and Huaping Li
Biomolecules 2024, 14(3), 329; https://doi.org/10.3390/biom14030329 - 10 Mar 2024
Cited by 4 | Viewed by 2599
Abstract
Hyperglycemia in pregnancy (HIP) is linked to fetoplacental endothelial dysfunction, which might be a result of hyperglycemia. Hyperglycemia is associated with cell senescence; however, the role and mechanism of high glucose and cell senescence in HIP endothelial cell failure are largely unknown. Our [...] Read more.
Hyperglycemia in pregnancy (HIP) is linked to fetoplacental endothelial dysfunction, which might be a result of hyperglycemia. Hyperglycemia is associated with cell senescence; however, the role and mechanism of high glucose and cell senescence in HIP endothelial cell failure are largely unknown. Our study discovered that human umbilical vein endothelial cells (HUVECs) obtained from HIP pregnant women exhibit excessive senescence, with significantly elevated expression of senescence markers senescence-associated beta-galactosidase (SA-β-gal), p16, p21, and p53. Subsequently, we found that exposing primary HUVECs and cell lines to high glucose resulted in an increase in the synthesis of these senescence indicators, similar to what had been observed in pregnant women with HIP. A replicate senescence model and stress-induced premature senescence (SIPS) model showed higher amounts of vascular damage indicators, including von Willebrand factor (vWF), chemotactic C-C motif chemokine ligand 2 (CCL2), intercellular adhesion molecule 1 (ICAM-1), along with the anti-apoptotic protein BCL2. However, lower expressions of the pro-apoptotic component BAX, in addition to defective proliferation and tubulogenesis, were seen. Further studies indicated that hyperglycemia can not only induce these alterations in HUVECs but also exacerbate the aforementioned changes in both aging HUVECs. The experiments outlined above have also been validated in pregnant women with HIP. Collectively, these data suggest that exposure to high glucose accelerates cell senescence-mediated vein endothelial cell dysfunction, including excessive inflammation, cell adhesion, impaired angiogenesis, and cell proliferation possibly contributing to pregnancy complications and adverse pregnancy outcomes. Full article
(This article belongs to the Special Issue Placental-Related Disorders of Pregnancy: 2nd Edition)
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