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Biomedicines
Special Issues
Pathogenesis and Treatment of Preeclampsia
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Pathogenesis and Treatment of Preeclampsia

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 4250

Special Issue Editors

Dr. Patrizia Vergani

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, University of Milano-Bicocca, 20900 Monza, Italy
Interests: maternal–fetal medicine; high risk pregnancy; prenatal diagnosis; placental angiogenic markers
Dr. Valentina Giardini

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, IRCCS San Gerardo dei Tintori Foundation, University of Milano-Bicocca, 20900 Monza, Italy
Interests: angiogenic markers (PlGF and sFlt-1); preeclampsia; maternal–fetal medicine

Special Issue Information

Dear Colleagues,

Preeclampsia is a pregnancy-specific hypertensive disorder with multisystem involvement. It is one of the “great obstetrical syndromes” with multiple etiologic factors that converge to an angiogenic imbalance, such as endothelial dysfunction.

Preeclampsia complicates 5–8% of pregnancies worldwide and is one of the main causes of maternal and perinatal morbidity and mortality. Despite the increase in knowledge of its pathogenesis, there is no specific cure for this disease, other than delivery. Therefore, there is an urgent need for therapeutic strategies to prolong pregnancy in the case of early-onset forms and to prevent/reduce maternal–fetal–neonatal complications.

This Special Issue aims to collate research that explores all potential therapies for the prevention and treatment of preeclampsia, in the light of new etiopathogenetic evidence.

Dr. Patrizia Vergani
Dr. Valentina Giardini
Guest Editors

Manuscript Submission Information

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Keywords

  • preeclampsia
  • hypertensive disorders of pregnancy
  • placental dysfunction
  • endothelial dysfunction
  • therapy
  • angiogenic imbalance

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Published Papers (3 papers)

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Research

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16 pages, 3498 KiB  
Article
Neutralization of Marinobufagenin Demonstrates Efficacy In Vitro and In Vivo in Models of Pre-Eclampsia
by Ahmed F. Pantho, Mehruba Zaman, Syeda H. Afroze, John M. Wages, Bo Yu, James W. Larrick, Thomas J. Kuehl, Niraj Vora and Mohammad Nasir Uddin
Biomedicines 2025, 13(4), 782; https://doi.org/10.3390/biomedicines13040782 - 24 Mar 2025
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Abstract
Background/Objectives: Marinobufagenin (MBG) is a biomarker that is found to be high in pre-eclampsia (preE), and thus is relevant in the pathogenesis of obstetric complications. MBG is thought to possibly be implicated in harmful signaling within cytotrophoblasts (CTBs) of the placenta. In [...] Read more.
Background/Objectives: Marinobufagenin (MBG) is a biomarker that is found to be high in pre-eclampsia (preE), and thus is relevant in the pathogenesis of obstetric complications. MBG is thought to possibly be implicated in harmful signaling within cytotrophoblasts (CTBs) of the placenta. In this study, we evaluated how anti-MBG human monoclonal antibody can alter cellular signaling in CTBs and in a rat model of preE. Methods: CTB cell proliferation, migration, and invasion as a result of MBG, both with and without anti-MBG present, were monitored via cell-based studies. Pro-angiogenic and anti-angiogenic factors in response to MBG with and without antibody were measured. Finally, we evaluated the lead anti-MBG antibody in comparison with the parent murine antibody in a rat model of preE. Results: CTB cells exposed to ≥1 nM MBG showed decreased (p < 0.05) proliferation, migration, and invasion, decreased secretion of VEGF and PIGF, and increased secretion of sFlt-1 and sEng. Pretreatment with anti-MBG significantly (p < 0.05) attenuated MBG-induced CTB dysfunction and modulation of VEGF, PIGF, sFlt-1, and sEng expression. In the rat model, anti-MBG treatment normalized blood pressure, reduced proteinuria, and eliminated fetal effects. Conclusions: MBG is a potential causative agent for preE, as it causes dysfunction in CTBs due to anti-angiogenic milieu. Our study suggests that anti-MBG antibody binds to MBG, neutralizing it and preventing downstream signaling in vitro. In a rat model of preE, treatment with anti-MBG antibody was effective at normalizing blood pressure, kidney function, and fetal birth weights. These data suggest that a human monoclonal antibody with high specificity and affinity for MBG has potential as a therapeutic agent for preE. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Preeclampsia)
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13 pages, 9683 KiB  
Article
Expression of IMP3 and LIN28A RNA-Binding Proteins in Placentas of Patients with Pre-Eclampsia with and without Severe Features
by Maja Barbaric, Katarina Vukojevic, Anita Kolobaric, Martina Orlovic Vlaho, Tanja Kresic and Violeta Soljic
Biomedicines 2024, 12(4), 879; https://doi.org/10.3390/biomedicines12040879 - 16 Apr 2024
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Abstract
Background: this study aimed to determine the expression of RNA-binding oncofetal proteins IMP3 and LIN28A in extravillous (EVT) and villous trophoblast (VT) cells of placentas from pre-eclamptic (PE) pregnancies to better understand the pathogenesis of PE. Methods: placental tissue of 10 patients with [...] Read more.
Background: this study aimed to determine the expression of RNA-binding oncofetal proteins IMP3 and LIN28A in extravillous (EVT) and villous trophoblast (VT) cells of placentas from pre-eclamptic (PE) pregnancies to better understand the pathogenesis of PE. Methods: placental tissue of 10 patients with PE with severe features, 10 patients with PE without severe features and 20 age-matched healthy pregnancy controls were analyzed by immunohistochemistry, double immunofluorescence and qPCR. Results: We found a decreased percentage of IMP3-positive EVT cells in PE with and without severe features compared to that of the healthy control (p < 0.001). IMP3 expression was significantly low in VT of PE placentas compared to that of the healthy control (p = 0.002). There was no significant difference in LIN28A expression between groups of PE and the control group. Additionally, we noticed the trend toward downregulation of IMP3 mRNA and LIN28A mRNA in severe PE compared to that of healthy controls. Conclusions: We demonstrated that IMP3 expression is decreased in EVT and VT cells of placentas from pregnancies complicated with both PE with and without severe features. However, additional functional investigations are needed to clarify the role of IMP3 as a potential therapeutic target in the management of PE. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Preeclampsia)
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Review

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28 pages, 2241 KiB  
Review
Novel Role of Pin1-Cis P-Tau-ApoE Axis in the Pathogenesis of Preeclampsia and Its Connection with Dementia
by Emmanuel Amabebe, Zheping Huang, Sukanta Jash, Balaji Krishnan, Shibin Cheng, Akitoshi Nakashima, Yitong Li, Zhixong Li, Ruizhi Wang, Ramkumar Menon, Xiao Zhen Zhou, Kun Ping Lu and Surendra Sharma
Biomedicines 2025, 13(1), 29; https://doi.org/10.3390/biomedicines13010029 - 26 Dec 2024
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Abstract
Preeclampsia (preE) is a severe multisystem hypertensive syndrome of pregnancy associated with ischemia/hypoxia, angiogenic imbalance, apolipoprotein E (ApoE)-mediated dyslipidemia, placental insufficiency, and inflammation at the maternal–fetal interface. Our recent data further suggest that preE is associated with impaired autophagy, vascular dysfunction, and proteinopathy/tauopathy [...] Read more.
Preeclampsia (preE) is a severe multisystem hypertensive syndrome of pregnancy associated with ischemia/hypoxia, angiogenic imbalance, apolipoprotein E (ApoE)-mediated dyslipidemia, placental insufficiency, and inflammation at the maternal–fetal interface. Our recent data further suggest that preE is associated with impaired autophagy, vascular dysfunction, and proteinopathy/tauopathy disorder, similar to neurodegenerative diseases such as Alzheimer’s disease (AD), including the presence of the cis stereo-isoform of phosphorylated tau (cis P-tau), amyloid-β, and transthyretin in the placenta and circulation. This review provides an overview of the factors that may lead to the induction and accumulation of cis P-tau-like proteins by focusing on the inactivation of peptidyl-prolyl cis–trans isomerase (Pin1) that catalyzes the cis to trans isomerization of P-tau. We also highlighted the novel role of the Pin1-cis P-tau-ApoE axis in the development of preE, and propagation of cis P-tau-mediated abnormal protein aggregation (tauopathy) from the placenta to cerebral tissues later in life, leading to neurodegenerative conditions. In the case of preE, proteinopathy/tauopathy may interrupt trophoblast differentiation and induce cell death, similar to the events occurring in neurons. These events may eventually damage the endothelium and cause systemic features of disorders such as preE. Despite impressive research and therapeutic advances in both fields of preE and neurodegenerative diseases, further investigation of Pin1-cis P-tau and ApoE-related mechanistic underpinnings may unravel novel therapeutic options, and new transcriptional and proteomic markers. This review will also cover genetic polymorphisms in the ApoE alleles leading to dyslipidemia induction that may regulate the pathways causing preE or dementia-like features in the reproductive age or later in life, respectively. Full article
(This article belongs to the Special Issue Pathogenesis and Treatment of Preeclampsia)
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