Influence of Estrogens on Uterine Vascular Adaptation in Normal and Preeclamptic Pregnancies

Mandalà, Maurizio

doi:10.3390/ijms21072592

Cited by 42 publications

(29 citation statements)

References 160 publications

(187 reference statements)

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“…The relationship between higher 2nd trimester estrogen levels and increased ASD risk is intriguing as estrogen is widely seen as an indicator of maternal and fetal health. Estradiol acts to preserve fetal viability during in utero stress through suppression of inflammation ( 278 , 279 ) and uterine artery dilation that increases oxygen and nutrient supply to the fetus ( 280 , 281 ). Estradiol also mediates several critical factors in neurodevelopment providing an overall neuroprotective benefit ( 162 ).…”

Section: Discussionmentioning

confidence: 99%

The Prenatal Hormone Milieu in Autism Spectrum Disorder

2021

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Though the etiology of autism spectrum disorder (ASD) remains largely unknown, recent findings suggest that hormone dysregulation within the prenatal environment, in conjunction with genetic factors, may alter fetal neurodevelopment. Early emphasis has been placed on the potential role of in utero exposure to androgens, particularly testosterone, to theorize ASD as the manifestation of an “extreme male brain.” The relationship between autism risk and obstetric conditions associated with inflammation and steroid dysregulation merits a much broader understanding of the in utero steroid environment and its potential influence on fetal neuroendocrine development. The exploration of hormone dysregulation in the prenatal environment and ASD development builds upon prior research publishing associations with obstetric conditions and ASD risk. The insight gained may be applied to the development of chronic adult metabolic diseases that share prenatal risk factors with ASD. Future research directions will also be discussed.

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Section: Discussionmentioning

confidence: 99%

The Prenatal Hormone Milieu in Autism Spectrum Disorder

2021

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“…Estrogens can also induce the anti-inflammatory phenotypes directly, which has been confirmed by several studies [ 40 , 44 , 45 ]. It is important that estrogen levels in PE are decreased [ 9 , 10 , 14 , 15 , 46 ]. Evidence that estrogens induce expression of their own cognate receptors has been presented by other authors [ 47 , 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Estrogen Receptor α by Decidual Macrophages in Preeclampsia

et al. 2021

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Preeclampsia is a gestation-associated hypertensive syndrome that threatens the life and health of the mother and the child. The condition is presumably caused by systemic failure with a strong involvement of innate immunity. In particular, it has been associated with flexible phenotypes of macrophages, which depend on the molecules circulating in the blood and tissue fluid, such as cytokines and hormones. This study aimed at a comparative evaluation of pro-inflammatory (TNFα) and anti-inflammatory (CD206, MMP9, HGF) markers, as well as the levels of estrogen receptor α, expressed by decidual macrophages in normal pregnancy and in patients with early- and late-onset preeclampsia. The tissue samples of decidua basalis were examined by immunohistochemistry and Western blotting. Isolation of decidual macrophages and their characterization were performed using cultural methods, flow cytometry and real-time PCR. Over 50% of the isolated decidual macrophages were positive for the pan-macrophage marker CD68. In the early-onset preeclampsia group, the levels of estrogen receptor α in decidua were significantly decreased. Furthermore, significantly decreased levels of HGF and CD206 were observed in both preeclampsia groups compared with the control group. The observed downregulation of estrogen receptor α, HGF and CD206 may contribute to the balance of pro- and anti-inflammatory macrophages and thereby to pathogenesis of preeclampsia.

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“…The observed surge in progesterone activates calcineurin, which in turn initiates pathways, such as Akt and its downstream targets, 83,84 and induces cardiac hypertrophy. 83 Estrogens, produced first by the corpus luteum and subsequently chiefly by the syncytiotrophoblast, impact uterine artery vasodilation and other cellular processes in remodeling of the uterine vasculature 85 to increase uteroplacental blood flow and reduce PVR. 53,54 These changes and other adaptations in the maternal renal and pulmonary systems work to increase blood volume and CO. 53 A recent study in a mouse model showed that PlGF is associated with systemic maternal cardiovascular adaptations to pregnancy.…”

Section: The Impact Of the Fetus On Maternal Cardiac Remodelingmentioning

confidence: 99%

An integrated model of preeclampsia: a multifaceted syndrome of the maternal cardiovascular-placental-fetal array

Cohen

Goldman‐Wohl

2022

American Journal of Obstetrics and Gynecology

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Maternal tolerance of the semiallogenic fetus necessitates conciliation of competing interests. Viviparity evolved with a placenta to mediate the needs of the fetus and maternal adaptation to the demands of pregnancy and to ensure optimal survival for both entities. The maternal-fetal interface is imagined as a 2-dimensional porous barrier between the mother and fetus, when in fact it is an intricate multidimensional array of tissues and resident and circulating factors at play, encompassing the developing fetus, the growing placenta, the changing decidua, and the dynamic maternal cardiovascular system. Pregnancy triggers dramatic changes to maternal hemodynamics to meet the growing demands of the developing fetus. Nearly a century of extensive research into the development and function of the placenta has revealed the role of placental dysfunction in the great obstetrical syndromes, among them preeclampsia. Recently, a debate has arisen questioning the primacy of the placenta in the etiology of preeclampsia, asserting that the maternal cardiovascular system is the instigator of the disorder. It was the clinical observation of the high rate of preeclampsia in hydatidiform mole that initiated the focus on the placenta in the etiology of the disease. Over many years of research, shallow trophoblast invasion with deficient remodeling of the maternal spiral arteries into vessels of higher capacitance and lower resistance has been recognized as hallmarks of the preeclamptic milieu. The lack of the normal decrease in uterine artery resistance is likewise predictive of preeclampsia. In abdominal pregnancies, however, an extrauterine pregnancy develops without remodeling of the spiral arteries, yet there is reduced resistance in the uterine arteries and distant vessels, such as the maternal ophthalmic arteries. Proponents of the maternal cardiovascular model of preeclampsia point to the observed maternal hemodynamic adaptations to pregnancy and maladaptation in gestational hypertension and preeclampsia and how the latter resembles the changes associated with cardiac disease states. Recognition of the importance of the angiogenic-antiangiogenic balance between placental-derived growth factor and its receptor soluble fms-like tyrosine kinase-1 and disturbance in this balance by an excess of a circulating isoform, soluble fms-like tyrosine kinase-1, which competes for and disrupts the proangiogenic receptor binding of the vascular endothelial growth factor and placental-derived growth factor, opened new avenues of research into the pathways to normal adaptation of the maternal cardiovascular and other systems to pregnancy and maladaptation in preeclampsia. The significance of the "placenta vs heart" debate goes beyond the academic: understanding the mutuality of placental and maternal cardiac etiologies of preeclampsia has far-reaching clinical implications for designing prevention strategies, such as aspirin therapy, prediction and surveillance through maternal hemodynamic studies or serum placental-derived growth factor a...

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Influence of Estrogens on Uterine Vascular Adaptation in Normal and Preeclamptic Pregnancies

Cited by 42 publications

References 160 publications

The Prenatal Hormone Milieu in Autism Spectrum Disorder

The Prenatal Hormone Milieu in Autism Spectrum Disorder

Expression of Estrogen Receptor α by Decidual Macrophages in Preeclampsia

An integrated model of preeclampsia: a multifaceted syndrome of the maternal cardiovascular-placental-fetal array

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