A “cure” for preeclampsia: Improving neonatal outcomes by overcoming excess fetal placental vascular resistance

Byrne, Timothy

doi:10.1016/j.mehy.2015.06.001

Cited by 3 publications

(3 citation statements)

References 129 publications

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“…Furthermore, the placental vasculature is thought to exist at near maximal vasodilation under healthy conditions [35]. Changes in the function of placental vascular smooth muscle, including changes in differentiation, viability, and contractility, have been identified as predictors for reduced circulation, ischemia, and negative pregnancy and neonatal outcomes [24,36,37]. Interestingly, in our investigations we found that HUASMC have sustained expression of GPR18 under varied inflammatory stimuli (LPS or cytomix cocktail), and that treatment with RvD2 led to reduced responsiveness to LPS stimulation as measured by IL-6 inflammatory cytokine release.…”

Section: Discussionmentioning

confidence: 99%

Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

Ulu

Sahoo

Yuil‐Valdes

et al. 2019

IJMS

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Omega-3 fatty acids are important to pregnancy and neonatal development and health. One mechanism by which omega-3 fatty acids exert their protective effects is through serving as substrates for the generation of specialized pro-resolving lipid mediators (SPM) that potently limit and resolve inflammatory processes. We recently identified that SPM levels are increased in maternal blood at delivery as compared to umbilical cord blood, suggesting the placenta as a potential site of action for maternal SPM. To explore this hypothesis, we obtained human placental samples and stained for the SPM resolvin D2 (RvD2) receptor GPR18 via immunohistochemistry. In so doing, we identified GPR18 expression in placental vascular smooth muscle and extravillous trophoblasts of the placental tissues. Using in vitro culturing, we confirmed expression of GPR18 in these cell types and further identified that stimulation with RvD2 led to significantly altered responsiveness (cytoskeletal changes and pro-inflammatory cytokine production) to lipopolysaccharide inflammatory stimulation in human umbilical artery smooth muscle cells and placental trophoblasts. Taken together, these findings establish a role for SPM actions in human placental tissue.

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Section: Discussionmentioning

confidence: 99%

Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

Ulu

Sahoo

Yuil‐Valdes

et al. 2019

IJMS

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“…In addition, Byrne suggested that therapies for pulmonary hypertension to lower placental vascular resistance could be trialed for treatments in PE, as based on molecular similarities in hypoxic responses between placental and pulmonary vascular networks. 38 However, neither review expressed the hypothesis that studies of the placenta may provide a novel adjunct research tool for understanding fetal lung disease. Thus, studies of placental physiology in normal and pathological pregnancies may define mechanisms that could lead to new insights into fetal lung disease and links between placenta and lung disease after birth.…”

Section: Parallels Between Placental and Fetal Lung Diseasementioning

confidence: 99%

“…39 This concept has been explored in several studies examining placental responses to hypoxia 40 and also summarized in a recent review highlighting parallels in the physiology of pulmonary hypertension and the placental vascular responses to PE. 38 At the molecular level, a vasoconstrictor response to hypoxia may be directed by oxygen sensing potassium channels in vascular smooth muscle cells. 41 A variety of studies have demonstrated that in a hypoxic environment, oxygen sensing potassium channels have decreased activity leading to membrane depolarization, intracellular calcium influx and ultimately vasoconstriction.…”

Section: Parallels Between Placental and Fetal Lung Diseasementioning

confidence: 99%

Recent advances in antenatal factors predisposing to bronchopulmonary dysplasia

Taglauer¹,

Abman²,

Keller

2018

Seminars in Perinatology

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Bronchopulmonary dysplasia (BPD) remains a major cause of late morbidities and death after preterm birth. BPD is characterized by an arrest of vascular and alveolar growth and high risk for pulmonary hypertension; yet mechanisms contributing to its pathogenesis and early strategies to prevent BPD are poorly understood. Strong epidemiologic studies have shown that the “new BPD” reflects the long-lasting impact of antenatal factors on lung development, partly due to placental dysfunction, as reflected in recent data from animal models. Improved understanding of mechanisms through which antenatal stress alters placental function and contributes to BPD may lead to preventive therapies.

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Vascular reactivity is altered in the placentas of fetuses with congenital diaphragmatic hernia

Horn-Oudshoorn,

Broekhuizen,

Harhangi

et al. 2024

Placenta

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A “cure” for preeclampsia: Improving neonatal outcomes by overcoming excess fetal placental vascular resistance

Cited by 3 publications

References 129 publications

Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

Recent advances in antenatal factors predisposing to bronchopulmonary dysplasia

Vascular reactivity is altered in the placentas of fetuses with congenital diaphragmatic hernia

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