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This Special Issue on the "Molecular and Cellular Mechanisms of Preeclampsia" belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics" of the International Journal of Molecular Sciences. It was a very successful Special Issue as it contains 20 published papers, including one editorial, nine original research papers, and ten reviews on the topic. The original publications cover a wide spectrum of topics, including alterations and involvement of specific factors during preeclampsia, new non-invasive technologies to identify changes, new treatment options, animal models, gender aspects, and effects of the pregnancy pathology later in life. The review publications again cover a wide spectrum of topics, including factors and pathways involved in preeclampsia, effects on the maternal vascular and immune systems, effects on the placenta and the trophoblast, epigenetic changes, new preventive strategies, and new views on the current hypotheses on preeclampsia. Taken together, this Special Issue gives a fantastic overview on a broad spectrum of topics, all of which are important to identify the real etiology of preeclampsia and to finally develop real treatment options.
This Special Issue on the “Molecular and Cellular Mechanisms of Preeclampsia” belongs to the section “Molecular Pathology, Diagnostics, and Therapeutics” of the International Journal of Molecular Sciences. It was a very successful Special Issue as it contains 20 published papers, including one editorial, nine original research papers, and ten reviews on the topic. The original publications cover a wide spectrum of topics, including alterations and involvement of specific factors during preeclampsia, new non-invasive technologies to identify changes, new treatment options, animal models, gender aspects, and effects of the pregnancy pathology later in life. The review publications again cover a wide spectrum of topics, including factors and pathways involved in preeclampsia, effects on the maternal vascular and immune systems, effects on the placenta and the trophoblast, epigenetic changes, new preventive strategies, and new views on the current hypotheses on preeclampsia. Taken together, this Special Issue gives a fantastic overview on a broad spectrum of topics, all of which are important to identify the real etiology of preeclampsia and to finally develop real treatment options.
Discover new concepts in cardiovascular and hemodynamic functionality in feto-maternal medicine, from leading experts in the field.
This textbook aims to describe physiological and pathophysiological mechanisms that underlie human maternal-fetal interactions. The book emphasizes the structure and development of the fetoplacental unit, the endocrine and nutritional regulation of fetal development, nitric oxide signalling, solute carriers function and ion channels regulation in healthy pregnancies and diseases, like preeclampsia, gestational diabetes, and maternal obesity, among others. Also, we highlight novel mechanisms associated with language impairment in children, the use of serotonin inhibitors or cannabis during pregnancy, and maternal conditions' potential impact on cerebrovascular development in newborns and infants. The cellular and molecular understanding of maternal-fetal physiology and pathophysiology will allow the readers to understand the impact of diseases or conditions that are highly prevalent in pregnant women.
The placenta is an organ that connects the developing fetus to the uterine wall, thereby allowing nutrient uptake, waste elimination, and gas exchange via the mother's blood supply. Proper vascular development in the placenta is fundamental to ensuring a healthy fetus and successful pregnancy. This book provides an up-to-date summary and synthesis of knowledge regarding placental vascular biology and discusses the relevance of this vascular bed to the functions of the human placenta.
Preeclampsia (PE) is characterized by endothelial cell (EC) dysfunction, loss of vasodilatory capacity, and loss of EC integrity. In a healthy pregnancy, there is a 'normal' increase in inflammatory factors, including TNF-[alpha]. TNF-[alpha] abundance increases beyond compensatory limits in PE. The first aim examined the requirement of SRC (using inhibitors PP2, PP3, SRC-I1, Dasatinib*, Saracatinib*, *denotes clinical inhibitor), MEK (using inhibitors U0126, PD98059, PD0325901), and P38MAPK (using inhibitors SB203580, BIRB0796) in maintaining resistance (a hallmark of EC integrity) in P-UAECs via ECIS in the absence and presence of TNF-[alpha]. Our results showed that these inhibitors (and combinations) have differential responses in the absence and presence of TNF-[alpha]. While some inhibitors (and combinations) were stimulatory in the absence, none were able to provide complete or full protection in the presence of TNF-[alpha]-mediated destruction. We concluded the resistance of the P-UAEC monolayer is regulated by SRC, MEK, and P38MAPK. The second aim was to identify the effect of other inflammatory mediators, including interleukin 1[beta] (IL-1[beta]), interleukin 6 (IL-6), and interleukin 8 (IL-8) in the absence and presence of TNF-[alpha] (using P-UAECs via ECIS). In addition, we attempted to discern the effects of GP130 and the downstream signaling pathway JAK (using inhibitor AG490) and SRC (using inhibitor PP2) on EC integrity in the absence and presence of TNF-[alpha], IL-1[beta], or TNF+IL-1[beta]. In the absence of TNF-[alpha] several inhibitors (or combinations) increased resistances above control. However, none of the agents tested (alone or in combination) could prevent or provide full rescue of P-UAEC integrity from the effects of TNF-[alpha] alone or the IL-1[beta]+TNF-[alpha] combination. We conclude that while IL-1[beta] and TNF-[alpha] share some signaling pathways, they are clearly under distinct mechanisms of control. In the third and final aim, we examined if P-UAECs undergo cell surface changes (a process known as immune modulation) in response to long-term exposure (20hrs) to different cytokines TNF-[alpha] , IL-1[beta], or IFN-[gamma] and identify if there were subpopulations of cells (using multiparameter flow cytometry experiments). The novel discovery of this collection of work is that PUAEC subpopulations were formed and changes of these populations depend upon the type of cytokine treatment. Immune modulation is indeed at play in regulating endothelial subpopulations, damage, and, therefore, the pathogenesis of preeclampsia.
Chesley’s Hypertensive Disorders in Pregnancy continues its tradition as one of the beacons to guide the field of preeclampsia research, recognized for its uniqueness and utility. Hypertensive disorders remain one the major causes of maternal and fetal morbidity and death. It is also a leading cause of preterm birth now known to be a risk factor in remote cardiovascular disease. Despite this the hypertensive disorders remain marginally studied and management is often controversial. The fourth edition of Chesley’s Hypertensive Disorders in Pregnancy focuses on prediction, prevention, and management for clinicians, and is an essential reference text for clinical and basic investigators alike. Differing from other texts devoted to preeclampsia, it covers the whole gamut of high blood pressure, and not just preeclampsia. Features new chapters focusing on recent discoveries in areas such as fetal programming, genomics/proteomics, and angiogenesis Includes extensive updates to chapters on epidemiology, etiological considerations, pathophysiology, prediction, prevention, and management Discusses the emerging roles of metabolic syndrome and obesity and the increasing incidence of preeclampsia Each section overseen by one of the editors; each chapter co-authored by one of the editors, ensuring coherence throughout book
The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References