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Immune Mechanisms Mediating Hypertension and/or Intrauterine Growth Restriction (IUGR) during Pregnancy

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Obstetrics & Gynecology".

Deadline for manuscript submissions: closed (1 November 2021) | Viewed by 7527

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Special Issue Editor

Prof. Dr. Babbette LaMarca

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Guest Editor

1. Department of Pharmacology, University of Mississippi Medical Center, Jackson, MS, USA
2. Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, USA
Interests: pathophysiology of hypertension; placental ischemia; preeclampsia; hypertension during pregnancy; immune mechanisms of hypertension

Special Issue Information

Dear Colleagues,

Hypertensive disorders of pregnancy continue to rise worldwide! Preeclampsia is the leading cause of maternal and fetal mortality and morbidity in the US and many other countries around the globe. JCM announces a Special Issue titled Immune Mechanisms Mediating Hypertension and/or Intrauterine Growth Restriction (IUGR) during Pregnancy, and we invite your top notch research articles investigating immune molecules and cells that result in the important clinical features of these diseases. In addition, articles examining how anti-inflammatory therapies could improve pregnancy outcomes in clinical studies of this disease will be considered. Topics can include how inflammatory factors impact multiorgan dysfunction that involves placental, renal, hepatic, cardiovascular, endothelial or neurological deficits, leading to the clincial characteristics of preeclampsia and or IUGR. Studies of the long-term effects on neurological and cardiovascular function in mothers and their offspring are welcome.

Prof. Dr. Babbette LaMarca
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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

inflammation
hypertension
neuroinflammation
fetal growth restriction
preeclampsia

Published Papers (3 papers)

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Research

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12 pages, 16972 KiB

Open AccessArticle

Loss of E-Cadherin Staining Continuity in the Trophoblastic Basal Membrane Correlates with Increased Resistance in Uterine Arteries and Proteinuria in Patients with Pregnancy-Induced Hypertension

by Marta Pęksa, Alexandra Kamieniecki, Anna Gabrych, Anna Lew-Tusk, Krzysztof Preis and Małgorzata Świątkowska-Freund

J. Clin. Med. 2022, 11(3), 668; https://doi.org/10.3390/jcm11030668 - 27 Jan 2022

Cited by 5 | Viewed by 1685

Abstract

Pregnancy-induced hypertension (PIH), especially when complicated with pre-eclampsia (PE), could be a life-threatening complication of pregnancy. Pre-eclampsia is one of the leading causes of perinatal morbidity and mortality in women. Pre-eclampsia is mainly characterized by hypertension and kidney damage with proteinuria. Abnormal placentation and altered structure of the placental barrier are believed to participate in the pathogenesis of pregnancy-induced hypertension, leading to PE. In the current study, we aimed to analyze the immunohistochemical expression pattern of E-cadherin and p120, two markers of epithelial–mesenchymal transition, in placental samples derived from a group of 55 patients with pregnancy-induced hypertension, including pre-eclampsia and 37 healthy pregnant controls. The results were correlated with the presence of an obtained early uterine artery flow notching during diastole on Doppler ultrasound. We observed a higher frequency of discontinuous E-cadherin staining in the basement membrane of syncytiotrophoblast in patients with PIH/PE compared to controls (p < 0.001, Fisher’s exact test). Moreover, the loss of continuity of E-cadherin expression correlated with the presence of a bilateral early diastolic notch on Doppler ultrasound (p < 0.001, Fisher’s exact test) and the presence of proteinuria (p = 0.013, Fisher’s exact test). These findings suggest that E-cadherin contributes to the integrity of the placental barrier, and its loss could be an immunohistochemical marker of PE. Full article

(This article belongs to the Special Issue Immune Mechanisms Mediating Hypertension and/or Intrauterine Growth Restriction (IUGR) during Pregnancy)

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12 pages, 13307 KiB

Open AccessArticle

Characterization of Mitochondrial Bioenergetics in Preeclampsia

by Ramana Vaka, Evangeline Deer, Mark Cunningham, Kristen M. McMaster, Kedra Wallace, Denise C. Cornelius, Lorena M. Amaral and Babbette LaMarca

J. Clin. Med. 2021, 10(21), 5063; https://doi.org/10.3390/jcm10215063 - 29 Oct 2021

Cited by 12 | Viewed by 2460

Abstract

Preeclampsia (PE) is characterized by new onset hypertension during pregnancy and is associated with oxidative stress, placental ischemia, and autoantibodies to the angiotensin II type I receptor (AT1-AA). Mitochondrial (mt) dysfunction in PE and various sources of oxidative stress, such as monocytes, neutrophils, and CD4 + T cells, have been identified as important players in the pathophysiology of PE. We have established the significance of AT1-AA, TNF-α, and CD4 + T cells in causing mitochondrial (mt) dysfunction in renal and placental tissues in pregnant rats. Although the role of mt dysfunction from freshly isolated intact placental mitochondria has been compared in human PE and normally pregnant (NP) controls, variations among preterm PE or term PE have not been compared and mechanisms contributing to mt ROS during PE are unclear. Therefore, we hypothesized PE placentas would exhibit impaired placental mt function, which would be worse in preterm PE patients than in those of later gestational ages. Immediately after delivery, PE and NP patient’s placentas were collected, mt were isolated and mt respiration and ROS were measured. PE patients at either < or >34 weeks gestational age (GA) exhibited elevated blood pressure and decreased placental mt respiration rates (state 3 and maximal). Patients delivering at >34 weeks exhibited decreased Complex IV activity and expression. Placental mtROS was significantly reduced in both PE groups, compared to NP placental mitochondria. Collectively, the study demonstrates that PE mt dysfunction occurs in the placenta, with mtROS being lower than that seen in NP controls. These data indicate why antioxidants, as a potential target or new therapeutic agent, may not be ideal in treating the oxidative stress associated with PE. Full article

(This article belongs to the Special Issue Immune Mechanisms Mediating Hypertension and/or Intrauterine Growth Restriction (IUGR) during Pregnancy)

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Review

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14 pages, 1134 KiB

Open AccessReview

The Complement System, T Cell Response, and Cytokine Shift in Normotensive versus Pre-Eclamptic and Lupus Pregnancy

by Eugen Ancuța, Radu Zamfir, Gabriel Martinescu, Dragoș Valentin Crauciuc and Codrina Ancuța

J. Clin. Med. 2021, 10(24), 5722; https://doi.org/10.3390/jcm10245722 - 7 Dec 2021

Cited by 4 | Viewed by 2763

Abstract

Successful pregnancy requires an immunological shift with T helper CD4⁺ bias based on disbalance Th1/Th17 versus Th2/T regulatory (Tregs) required to induce tolerance against the semi-allogeneic fetus and placenta and to support fetal growth. Considered a pregnancy-specific hypertensive disorder, pre-eclampsia is characterized by multifaceted organ involvement related to impaired maternal immune tolerance to paternal antigens triggered by hypoxic placental injury as well as excessive local and systemic anti-angiogenic and inflammatory factor synthesis. Both systemic and local Th1/Th2 shift further expands to Th17 cells and their cytokines (IL-17) complemented by suppressive Treg and Th2 cytokines (IL-10, IL-4); alterations in Th17 and Tregs cause hypertension during pregnancy throughout vasoactive factors and endothelial dysfunction, providing an explanatory link between immunological and vascular events in the pathobiology of pre-eclamptic pregnancy. Apart from immunological changes representative of normotensive pregnancy, lupus pregnancy is generally defined by higher serum pro-inflammatory cytokines, lower Th2 polarization, defective and lower number of Tregs, potential blockade of complement inhibitors by anti-phospholipid antibodies, and similar immune alterations to those seen in pre-eclampsia. The current review underpins the immune mechanisms of pre-eclampsia focusing on local (placental) and systemic (maternal) aberrant adaptive and innate immune response versus normotensive pregnancy and pregnancy in systemic autoimmune conditions, particularly lupus. Full article

(This article belongs to the Special Issue Immune Mechanisms Mediating Hypertension and/or Intrauterine Growth Restriction (IUGR) during Pregnancy)

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