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Genetic and Epigenetic Regulation of Placental Development and Disease
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Genetic and Epigenetic Regulation of Placental Development and Disease

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 19780

Special Issue Editors

Prof. Dr. Nihar R Nayak

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Guest Editor
Department of Obstetrics and Gynecology, UMKC School of Medicine, Kansas City, MO 64108, USA
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Gary Sutkin

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Guest Editor
Department of Biomedical and Health Informatics, Obstetrics and Gynecology, UMKC School of Medicine, Kansas City, MO 64108, USA
Interests: gynecology
Special Issues, Collections and Topics in MDPI journals
Dr. Sunil Jaiman

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Guest Editor
School of Medicine, Wayne State University, Detroit, MI 48201, USA
Interests: placental pathology-abruptio placenta; decidual vasculopathy; morbidly adherent placenta; placental response to infection; perinatal autopsy; development of the human placenta; disorders of placental villous maturation; placental contribution to fetal death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Precise regulation of placental gene expression at each stage of pregnancy is crucial for the successful establishment and maintenance of pregnancy. Dysregulation of these gene regulatory mechanisms during pregnancy has been implicated in most pregnancy complications, including preeclampsia, preterm birth, intrauterine growth restriction, abruptio placentae, and late spontaneous abortion, which have enormous impacts on the life-long health of mothers and the babies born to mothers with these conditions. However, the molecular underpinnings of placental developmental defects leading to such pregnancy complications are still poorly understood. By understanding the molecular pathways and the distinct defects in trophoblast development and differentiation associated with each pregnancy disease, we could develop much needed diagnostic, preventive, and therapeutic strategies for these diseases.

The goal of this Special Issue is to publish high-quality manuscripts with special emphasis on the genetic and epigenetic regulation of normal placental development and placental developmental defects leading to different pregnancy complications. We welcome reviews, new methods, short communications, and original articles covering all aspects of trophoblast development and differentiation and pregnancy diseases using culture models, clinical studies, and animal models. Priorities for publication will be given to studies related to the impact of DNA methylation, histone post-translational modifications, non-coding RNA (long non-coding RNA and microRNA), and epigenetic biomarkers for pregnancy diseases.

We look forward to your contributions.

Prof. Dr. Nihar R Nayak
Prof. Dr. Gary Sutkin
Prof. Dr. Sunil Jaiman
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. Genes 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

  • Placenta 
  • Trophoblast invasion 
  • Trophoblast differentiation 
  • Maternal–fetal interaction 
  • Spiral artery remodeling 
  • Vascular complications in pregnancy 
  • Pregnancy diseases 
  • Gene regulation 
  • Epigenetic regulation 
  • Biomarkers for pregnancy diseases 
  • Implantation 
  • Placental development

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Published Papers (7 papers)

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Research

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15 pages, 1757 KiB  
Article
Proteomic Profiling and Pathway Analysis of Acid Stress-Induced Vasorelaxation of Mesenteric Arteries In Vitro
by Ipsita Mohanty, Sudeshna Banerjee, Arabinda Mahanty, Sasmita Mohanty, Nihar Ranjan Nayak, Subas Chandra Parija and Bimal Prasanna Mohanty
Genes 2022, 13(5), 801; https://doi.org/10.3390/genes13050801 - 29 Apr 2022
Viewed by 2302
Abstract
Although metabolic acidosis is associated with numerous pathophysiological conditions and its vasorelaxation effects have been well described in different animal and culture models, the molecular mechanisms of acidosis-induced vasorelaxation are not fully understood. Mesenteric artery models have been used extensively to examine the [...] Read more.
Although metabolic acidosis is associated with numerous pathophysiological conditions and its vasorelaxation effects have been well described in different animal and culture models, the molecular mechanisms of acidosis-induced vasorelaxation are not fully understood. Mesenteric artery models have been used extensively to examine the vascular response to various pathophysiological conditions. Our previous studies and several other reports have suggested the vascular responses of goat mesenteric arteries and human arteries to various stimuli, including acidic stress, are highly similar. In this study, to further identify the signaling molecules responsible for altered vasoreactivity in response to acidic pH, we examined the proteomic profile of acid stress-induced vasorelaxation using a goat mesenteric artery model. The vascular proteomes under acidic pH were compared using 2D-GE with 7 cm IPG strips and mini gels, LC-MS/MS, and MALDI TOF MS. The unique proteins identified by mass spectroscopy were actin, transgelin, WD repeat-containing protein 1, desmin, tropomyosin, ATP synthase β, Hsp27, aldehyde dehydrogenase, pyruvate kinase, and vitamin K epoxide reductase complex subunit 1-like protein. Out of five protein spots identified as actin, three were upregulated > 2-fold. ATP synthase β was also upregulated (2.14-fold) under acid stress. Other actin-associated proteins upregulated were transgelin, desmin, and WD repeat-containing protein 1. Isometric contraction studies revealed that both receptor-mediated (histamine) and non-receptor-mediated (KCl) vasocontraction were attenuated, whereas acetylcholine-induced vasorelaxation was augmented under acidosis. Overall, the altered vasoreactivity under acidosis observed in the functional studies could possibly be attributed to the increase in expression of actin and ATP synthase β. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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14 pages, 4774 KiB  
Article
Glutamate Uptake Is Not Impaired by Hypoxia in a Culture Model of Human Fetal Neural Stem Cell-Derived Astrocytes
by Vadanya Shrivastava, Devanjan Dey, Chitra Mohinder Singh Singal, Paritosh Jaiswal, Ankit Singh, Jai Bhagwan Sharma, Parthaprasad Chattopadhyay, Nihar Ranjan Nayak, Jayanth Kumar Palanichamy, Subrata Sinha, Pankaj Seth and Sudip Sen
Genes 2022, 13(3), 506; https://doi.org/10.3390/genes13030506 - 12 Mar 2022
Cited by 2 | Viewed by 3070
Abstract
Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the molecular mechanisms, and roles of various [...] Read more.
Hypoxic ischemic injury to the fetal and neonatal brain is a leading cause of death and disability worldwide. Although animal and culture studies suggest that glutamate excitotoxicity is a primary contributor to neuronal death following hypoxia, the molecular mechanisms, and roles of various neural cells in the development of glutamate excitotoxicity in humans, is not fully understood. In this study, we developed a culture model of human fetal neural stem cell (FNSC)-derived astrocytes and examined their glutamate uptake in response to hypoxia. We isolated, established, and characterized cultures of FNSCs from aborted fetal brains and differentiated them into astrocytes, characterized by increased expression of the astrocyte markers glial fibrillary acidic protein (GFAP), excitatory amino acid transporter 1 (EAAT1) and EAAT2, and decreased expression of neural stem cell marker Nestin. Differentiated astrocytes were exposed to various oxygen concentrations mimicking normoxia (20% and 6%), moderate and severe hypoxia (2% and 0.2%, respectively). Interestingly, no change was observed in the expression of the glutamate transporter EAAT2 or glutamate uptake by astrocytes, even after exposure to severe hypoxia for 48 h. These results together suggest that human FNSC-derived astrocytes can maintain glutamate uptake after hypoxic injury and thus provide evidence for the possible neuroprotective role of astrocytes in hypoxic conditions. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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15 pages, 2598 KiB  
Article
Effects of Maternal Diabetes and Diet on Gene Expression in the Murine Placenta
by Claudia Kappen, Claudia Kruger and J. Michael Salbaum
Genes 2022, 13(1), 130; https://doi.org/10.3390/genes13010130 - 12 Jan 2022
Cited by 6 | Viewed by 2420
Abstract
Adverse exposures during pregnancy have been shown to contribute to susceptibility for chronic diseases in offspring. Maternal diabetes during pregnancy is associated with higher risk of pregnancy complications, structural birth defects, and cardiometabolic health impairments later in life. We showed previously in a [...] Read more.
Adverse exposures during pregnancy have been shown to contribute to susceptibility for chronic diseases in offspring. Maternal diabetes during pregnancy is associated with higher risk of pregnancy complications, structural birth defects, and cardiometabolic health impairments later in life. We showed previously in a mouse model that the placenta is smaller in diabetic pregnancies, with reduced size of the junctional zone and labyrinth. In addition, cell migration is impaired, resulting in ectopic accumulation of spongiotrophoblasts within the labyrinth. The present study had the goal to identify the mechanisms underlying the growth defects and trophoblast migration abnormalities. Based upon gene expression assays of 47 candidate genes, we were able to attribute the reduced growth of diabetic placenta to alterations in the Insulin growth factor and Serotonin signaling pathways, and provide evidence for Prostaglandin signaling deficiencies as the possible cause for abnormal trophoblast migration. Furthermore, our results reinforce the notion that the exposure to maternal diabetes has particularly pronounced effects on gene expression at midgestation time points. An implication of these findings is that mechanisms underlying developmental programming act early in pregnancy, during placenta morphogenesis, and before the conceptus switches from histiotrophic to hemotrophic nutrition. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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15 pages, 3917 KiB  
Article
Characterization of Copy-Number Variations and Possible Candidate Genes in Recurrent Pregnancy Losses
by Yan-Ran Sheng, Shun-Yu Hou, Wen-Ting Hu, Chun-Yan Wei, Yu-Kai Liu, Yu-Yin Liu, Lu Jiang, Jing-Jing Xiang, Xiao-Xi Sun, Cai-Xia Lei, Hui-Ling Wang and Xiao-Yong Zhu
Genes 2021, 12(2), 141; https://doi.org/10.3390/genes12020141 - 22 Jan 2021
Cited by 17 | Viewed by 3218
Abstract
It is well established that embryonic chromosomal abnormalities (both in the number of chromosomes and the structure) account for 50% of early pregnancy losses. However, little is known regarding the potential differences in the incidence and distribution of chromosomal abnormalities between patients with [...] Read more.
It is well established that embryonic chromosomal abnormalities (both in the number of chromosomes and the structure) account for 50% of early pregnancy losses. However, little is known regarding the potential differences in the incidence and distribution of chromosomal abnormalities between patients with sporadic abortion (SA) and recurrent pregnancy loss (RPL), let alone the role of submicroscopic copy-number variations (CNVs) in these cases. The aim of the present study was to systematically evaluate the role of embryonic chromosomal abnormalities and CNVs in the etiology of RPL compared with SA. Over a 3-year period, 1556 fresh products of conception (POCs) from miscarriage specimens were investigated using single nucleotide polymorphism array (SNP-array) and CNV sequencing (CNV-seq) in this study, along with further functional enrichment analysis. Chromosomal abnormalities were identified in 57.52% (895/1556) of all cases. Comparisons of the incidence and distributions of chromosomal abnormalities within the SA group and RPL group and within the different age groups were performed. Moreover, 346 CNVs in 173 cases were identified, including 272 duplications, 2 deletions and 72 duplications along with deletions. Duplications in 16q24.3 and 16p13.3 were significantly more frequent in RPL cases, and thereby considered to be associated with RPL. There were 213 genes and 131 signaling pathways identified as potential RPL candidate genes and signaling pathways, respectively, which were centered primarily on six functional categories. The results of the present study may improve our understanding of the etiologies of RPL and assist in the establishment of a population-based diagnostic panel of genetic markers for screening RPL amongst Chinese women. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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Review

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19 pages, 1910 KiB  
Review
Paralogous Genes Involved in Embryonic Development: Lessons from the Eye and other Tissues
by Michaela Drobek
Genes 2022, 13(11), 2082; https://doi.org/10.3390/genes13112082 - 9 Nov 2022
Cited by 1 | Viewed by 2934
Abstract
During evolution, gene duplications lead to a naturally increased gene dosage. Duplicated genes can be further retained or eliminated over time by purifying selection pressure. The retention probability is increased by functional diversification and by the acquisition of novel functions. Interestingly, functionally diverged [...] Read more.
During evolution, gene duplications lead to a naturally increased gene dosage. Duplicated genes can be further retained or eliminated over time by purifying selection pressure. The retention probability is increased by functional diversification and by the acquisition of novel functions. Interestingly, functionally diverged paralogous genes can maintain a certain level of functional redundancy and at least a partial ability to replace each other. In such cases, diversification probably occurred at the level of transcriptional regulation. Nevertheless, some duplicated genes can maintain functional redundancy after duplication and the ability to functionally compensate for the loss of each other. Many of them are involved in proper embryonic development. The development of particular tissues/organs and developmental processes can be more or less sensitive to the overall gene dosage. Alterations in the gene dosage or a decrease below a threshold level may have dramatic phenotypic consequences or even lead to embryonic lethality. The number of functional alleles of particular paralogous genes and their mutual cooperation and interactions influence the gene dosage, and therefore, these factors play a crucial role in development. This review will discuss individual interactions between paralogous genes and gene dosage sensitivity during development. The eye was used as a model system, but other tissues are also included. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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14 pages, 3494 KiB  
Review
Novel Technologies for Target Delivery of Therapeutics to the Placenta during Pregnancy: A Review
by Gerald J. Pepe and Eugene D. Albrecht
Genes 2021, 12(8), 1255; https://doi.org/10.3390/genes12081255 - 17 Aug 2021
Cited by 8 | Viewed by 3111
Abstract
Uterine spiral artery remodeling is essential for placental perfusion and fetal growth and, when impaired, results in placental ischemia and pregnancy complications, e.g., fetal growth restriction, preeclampsia, premature birth. Despite the high incidence of adverse pregnancies, current treatment options are limited. Accordingly, research [...] Read more.
Uterine spiral artery remodeling is essential for placental perfusion and fetal growth and, when impaired, results in placental ischemia and pregnancy complications, e.g., fetal growth restriction, preeclampsia, premature birth. Despite the high incidence of adverse pregnancies, current treatment options are limited. Accordingly, research has shifted to the development of gene therapy technologies that provide targeted delivery of “payloads” to the placenta while limiting maternal and fetal exposure. This review describes the current strategies, including placental targeting peptide-bound liposomes, nanoparticle or adenovirus constructs decorated with specific peptide sequences and placental gene promoters delivered via maternal IV injection, directly into the placenta or the uterine artery, as well as noninvasive site-selective targeting of regulating genes conjugated with microbubbles via contrast-enhanced ultrasound. The review also provides a perspective on the effectiveness of these technologies in various animal models and their practicability and potential use for targeted placental delivery of therapeutics and genes in adverse human pregnancies affected by placental dysfunction. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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10 pages, 257 KiB  
Review
Quantifying Fetal Reprogramming for Biomarker Development in the Era of High-Throughput Sequencing
by Fu-Sheng Chou, Krystel Newton and Pei-Shan Wang
Genes 2021, 12(3), 329; https://doi.org/10.3390/genes12030329 - 25 Feb 2021
Viewed by 1771
Abstract
Gestational hypertensive disorders continue to threaten the well-being of pregnant women and their offspring. The only current definitive treatment for gestational hypertensive disorders is delivery of the fetus. The optimal timing of delivery remains controversial. Currently, the available clinical tools do not allow [...] Read more.
Gestational hypertensive disorders continue to threaten the well-being of pregnant women and their offspring. The only current definitive treatment for gestational hypertensive disorders is delivery of the fetus. The optimal timing of delivery remains controversial. Currently, the available clinical tools do not allow for assessment of fetal stress in its early stages. Placental insufficiency and fetal growth restriction secondary to gestational hypertensive disorders have been shown to have long-term impacts on offspring health even into their adulthood, becoming one of the major focuses of research in the field of developmental origins of health and disease. Fetal reprogramming was introduced to describe the long-lasting effects of the toxic intrauterine environment on the growing fetus. With the advent of high-throughput sequencing, there have been major advances in research attempting to quantify fetal reprogramming. Moreover, genes that are found to be differentially expressed as a result of fetal reprogramming show promise in the development of transcriptional biomarkers for clinical use in detecting fetal response to placental insufficiency. In this review, we will review key pathophysiology in the development of placental insufficiency, existing literature on high-throughput sequencing in the study of fetal reprogramming, and considerations regarding research design from our own experience. Full article
(This article belongs to the Special Issue Genetic and Epigenetic Regulation of Placental Development and Disease)
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