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Novel Diagnostic and Preventive Options of Pregnancy Complications Originated from Placental Pathologies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 3385

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Special Issue Editors

Dr. Padma Murthi

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Guest Editor

1. Department of Pharmacology, Monash Biomedicine Discovery Institute, Monash University, Melbourne, VIC 3168, Australia
2. Department of Obstetrics and Gynecology, The University of Melbourne, Parkville, VIC 3010, Australia
Interests: placenta; preeclampsia; fetal medicine; fetal growth restriction; fetal development; placental insufficiency
Special Issues, Collections and Topics in MDPI journals

Dr. Nandor Gabor Than

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Guest Editor

Systems Biology of Reproduction Research Group, Institute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary
Interests: pregnancy; pregnancy complication; miscarriage; preeclampsia; gestational trophoblastic disease; placenta; placental protein; galectin; perinatology; reproductive biology; reproductive immunology; systems biology
Special Issues, Collections and Topics in MDPI journals

Dr. Offer Erez

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Guest Editor

Department of Obstetrics and Gynecology, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer Sheva 8410101, Israel
Interests: preeclampsia; preterm labor; coagulation during pregnancy; IUGR; preterm PROM

Special Issue Information

Dear Colleagues,

Placental dysfunction underlies major obstetric diseases including miscarriage, preterm birth, foetal growth-restriction, preeclampsia and stillbirth. Whilst there has been progress made in our understanding of the placental molecular pathways involved in the pathophysiology of these obstetrical syndromes, a significant gap still exists in utilizing this information collected thus far for the development of novel diagnostic and treatment modalities. This could mainly be attributed to the distinct subtypes of placental dysfunction presented with complex clinical phenotypes and resulting in heterogeneous patient populations. Therefore, this Special Issue is focused on inviting research papers to greatly enhance our understanding and knowledge on the different disease subtypes of the dysfunctional placenta that are associated with disorders of pregnancy and to suggest new venues in closing the gaps between the bench and the clinical practice. Such biomedical discoveries would significantly enhance the opportunities to develop novel and early diagnostic tools and tailored preventive therapies to improve maternal and foetal health outcomes during pregnancy and beyond.

Dr. Padma Murthi
Dr. Nandor Gabor Than
Dr. Offer Erez
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

placental dysfunction
disorders of pregnancy
maternal and foetal health

Published Papers (3 papers)

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Research

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23 pages, 3265 KiB

Open AccessArticle

Decreased Expression of Placental Proteins in Recurrent Pregnancy Loss: Functional Relevance and Diagnostic Value

by Eszter Tóth, Dániel Györffy, Máté Posta, Petronella Hupuczi, Andrea Balogh, Gábor Szalai, Gergő Orosz, László Orosz, András Szilágyi, Orsolya Oravecz, Lajos Veress, Sándor Nagy, Olga Török, Padma Murthi, Offer Erez, Zoltán Papp, Nándor Ács and Nándor Gábor Than

Int. J. Mol. Sci. 2024, 25(3), 1865; https://doi.org/10.3390/ijms25031865 - 03 Feb 2024

Cited by 1 | Viewed by 1035

Abstract

Miscarriages affect 50–70% of all conceptions and 15–20% of clinically recognized pregnancies. Recurrent pregnancy loss (RPL, ≥2 miscarriages) affects 1–5% of recognized pregnancies. Nevertheless, our knowledge about the etiologies and pathophysiology of RPL is incomplete, and thus, reliable diagnostic/preventive tools are not yet available. Here, we aimed to define the diagnostic value of three placental proteins for RPL: human chorionic gonadotropin free beta-subunit (free-β-hCG), pregnancy-associated plasma protein-A (PAPP-A), and placental growth factor (PlGF). Blood samples were collected from women with RPL (n = 14) and controls undergoing elective termination of pregnancy (n = 30) at the time of surgery. Maternal serum protein concentrations were measured by BRAHMS KRYPTOR Analyzer. Daily multiple of median (dMoM) values were calculated for gestational age-specific normalization. To obtain classifiers, logistic regression analysis was performed, and ROC curves were calculated. There were differences in changes of maternal serum protein concentrations with advancing healthy gestation. Between 6 and 13 weeks, women with RPL had lower concentrations and dMoMs of free β-hCG, PAPP-A, and PlGF than controls. PAPP-A dMoM had the best discriminative properties (AUC = 0.880). Between 9 and 13 weeks, discriminative properties of all protein dMoMs were excellent (free β-hCG: AUC = 0.975; PAPP-A: AUC = 0.998; PlGF: AUC = 0.924). In conclusion, free-β-hCG and PAPP-A are valuable biomarkers for RPL, especially between 9 and 13 weeks. Their decreased concentrations indicate the deterioration of placental functions, while lower PlGF levels indicate problems with placental angiogenesis after 9 weeks. Full article

(This article belongs to the Special Issue Novel Diagnostic and Preventive Options of Pregnancy Complications Originated from Placental Pathologies)

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17 pages, 14907 KiB

Open AccessArticle

mRNA and Protein Expression in Human Fetal Membrane Cells: Potential Biomarkers for Preterm Prelabor Rupture of the Fetal Membranes?

by Emmeli Mikkelsen, Berthold Huppertz, Ripudaman Singh, Katarina Ravn, Lotte Hatt, Mogens Kruhøffer, Rheanna Urrabaz-Garza, Niels Uldbjerg, Ramkumar Menon and Torben Steiniche

Int. J. Mol. Sci. 2023, 24(21), 15826; https://doi.org/10.3390/ijms242115826 - 31 Oct 2023

Viewed by 1084

Abstract

Clinically, unique markers in fetal membrane cells may contribute to the search for biomarkers for preterm prelabor rupture of the fetal membranes (pPROM) in maternal blood. pPROM is associated with overwhelming inflammation and premature cellular senescence causing “biological microfractures” of the fetal membranes. We hypothesize that these pathological processes are associated with the shedding of fetal membrane cells into the maternal circulation. The aim of this study was to identify markers expressed exclusively in fetal membrane cells to facilitate their isolation, characterization, and determination of biomarker potential in maternal blood. We have (1), by their transcriptomic profile, identified markers that are upregulated in amnion and chorion tissue compared to maternal white blood cells, and (2), by immunohistochemistry, confirmed the localization of the differentially expressed proteins in fetal membranes, placenta, and the placental bed of the uterus. RNA sequencing revealed 31 transcripts in the amnion and 42 transcripts in the chorion that were upregulated. Among these, 22 proteins were evaluated by immunohistochemistry. All but two transcripts were expressed both on mRNA and protein level in at least one fetal membrane cell type. Among these remaining 20 proteins, 9 proteins were not significantly expressed in the villous and extravillous trophoblasts of the placenta. Full article

(This article belongs to the Special Issue Novel Diagnostic and Preventive Options of Pregnancy Complications Originated from Placental Pathologies)

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Review

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13 pages, 2335 KiB

Open AccessReview

The Role of the Placental Enzyme Indoleamine 2,3-Dioxygenase in Normal and Abnormal Human Pregnancy

by Yoshiki Kudo and Jun Sugimoto

Int. J. Mol. Sci. 2024, 25(8), 4577; https://doi.org/10.3390/ijms25084577 - 22 Apr 2024

Viewed by 589

Abstract

The biologically significant phenomenon that the fetus can survive immune attacks from the mother has been demonstrated in mammals. The survival mechanism depends on the fetus and placenta actively defending themselves against attacks by maternal T cells, achieved through the localized depletion of the amino acid L-tryptophan by an enzyme called indoleamine 2,3-dioxygenase. These findings were entirely unexpected and pose important questions regarding diseases related to human pregnancy and their prevention during human pregnancy. Specifically, the role of this mechanism, as discovered in mice, in humans remains unknown, as does the extent to which impaired activation of this process contributes to major clinical diseases in humans. We have, thus, elucidated several key aspects of this enzyme expressed in the human placenta both in normal and abnormal human pregnancy. The questions addressed in this brief review are as follows: (1) localization and characteristics of human placental indoleamine 2,3-dioxygenas; (2) overall tryptophan catabolism in human pregnancy and a comparison of indoleamine 2,3-dioxygenase expression levels between normal and pre-eclamptic pregnancy; (3) controlling trophoblast invasion by indoleamine 2,3-dioxygenase and its relation to the pathogenesis of placenta accrete spectrum. Full article

(This article belongs to the Special Issue Novel Diagnostic and Preventive Options of Pregnancy Complications Originated from Placental Pathologies)

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