Arginine vasopressin infusion is sufficient to model clinical features of preeclampsia in mice

Sandgren, Jeremy A; Deng, Guorui; Linggonegoro, Danny W.; Scroggins, Sabrina M; Perschbacher, Katherine J; Nair, Anand; Nishimura, Taryn; Zhang, Shao Yang; Agbor, Larry N; Wu, Jing; Keen, Henry L.; Naber, Meghan C.; Pearson, Nicole A; Zimmerman, Kathy; Weiß, Robert M.; Bowdler, Noelle C.; Usachev, Yuriy M.; Santillan, Donna A.; Potthoff, Matthew J.; Pierce, Gary L.; Gibson‐Corley, Katherine N.; Sigmund, Curt D.; Santillan, Mark K.; Grobe, Justin L

doi:10.1172/jci.insight.99403

Cited by 61 publications

(73 citation statements)

References 114 publications

(102 reference statements)

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“…In addition, excess vasopressin has been implicated in the maternal disease in animal models of pre-eclampsia 142 . In clinical settings characterized by excess vasopressin, water excretion by the kidneys is substantially impaired, leading to severe hyponatraemia.…”

Section: Maternal Syndromementioning

confidence: 99%

Pre-eclampsia: pathogenesis, novel diagnostics and therapies

et al. 2019

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Pre-eclampsia is a complication of pregnancy that is associated with substantial maternal and fetal morbidity and mortality. The disease presents with new-onset hypertension and often proteinuria in the mother, which can progress to multi-organ dysfunction, including hepatic, renal and cerebral disease, if the fetus and placenta are not delivered. Maternal endothelial dysfunction due to circulating factors of fetal origin from the placenta is a hallmark of pre-eclampsia. Risk factors for the disease include maternal comorbidities, such as chronic kidney disease, hypertension and obesity; a family history of pre-eclampsia, nulliparity or multiple pregnancies; and previous preeclampsia or intrauterine fetal growth restriction. In the past decade, the discovery and characterization of novel antiangiogenic pathways have been particularly impactful both in increasing understanding of the disease pathophysiology and in directing predictive and therapeutic efforts. In this Review, we discuss the pathogenic role of antiangiogenic proteins released by the placenta in the development of pre-eclampsia and review novel therapeutic strategies directed at restoring the angiogenic imbalance observed during pre-eclampsia. We also highlight other notable advances in the field, including the identification of long-term maternal and fetal risks conferred by pre-eclampsia.

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Section: Maternal Syndromementioning

confidence: 99%

Pre-eclampsia: pathogenesis, novel diagnostics and therapies

et al. 2019

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“…Moreover, Copeptin, a marker of AVP secretion, is elevated throughout human and mice pregnancies complicated by preeclampsia [47]. Also, AVP infusion into pregnant mice resulted in hypertension, renal glomerular endotheliosis, intrauterine growth restriction, decreased placental growth factor (PGF), altered placental morphology, placental oxidative stress, and placental gene expression consistent with human preeclampsia [48].…”

Section: Discussionmentioning

confidence: 99%

Expression of Stress-Mediating Genes Is Increased in Term Placentas of Women with Chronic Self-Perceived Anxiety and Depression

Martínez¹,

Marteinsdóttir²,

Josefsson³

et al. 2020

Preprint

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Anxiety, chronical stress and depression during pregnancy are considered to affect the offspring, presumably through placental dysregulation. We have studied the term placentae of pregnancies clinically monitored with the Beck’s Anxiety Inventory (BAI) and Edinburgh Postnatal Depression Scale (EPDS). A cutoff threshold for BAI/EPDS of 10 classed patients into an Index group (>10, n=23) and a Control group (<10, n=23). Cortisol concentrations in hair (HCC) were periodically monitored throughout pregnancy and delivery. Expression differences of main glucocorticoid pathway genes: i.e. corticotropin-releasing hormone (CRH), 11β-hydroxysteroid dehydrogenase (HSD11B2), glucocorticoid receptor (NR3C1), as well as other key stress biomarkers (Arginine Vasopressin, AVP and O-GlcNAc transferase, OGT) were explored in medial placentae using real-time qPCR and western blotting. Moreover, gene expression changes were considered for their association with HCC, offspring, gender and birthweight. A significant dysregulation of gene expression for CRH, AVP and HSD11B2 genes was seen in the Index group, compared to controls, while OGT and NR3C1 expression remained similar between groups. Placental gene expression of the stress-modulating enzyme 11β-hydroxysteroid dehydrogenase (HSD11B2) was related to both hair cortisol levels (Rho= 0.54; p<0.01) and the sex of the newborn in pregnancies perceived as stressful (Index, p<0.05). Gene expression of CRH correlated with both AVP (Rho= 0.79; p<0.001) and HSD11B2 (Rho= 0.45; p<0.03), and also between AVP with both HSD11B2 (Rho= 0.6; p<0.005) and NR3C1 (Rho= 0.56; p<0.03) in the Control group but not in the Index group; suggesting a possible loss of interaction in the mechanisms of action of these genes under stress circumstances during pregnancy.

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“…Consistent with our results, AVP shows a peak of expression under fetal “stress” circumstances, such as heat stress, leading to widespread effects on fetal cardiovascular, renal, and lung functions [ 51 ]. The marker of AVP secretion Copeptin appears increased in pre-eclampsia, both in human and murine pregnancies [ 52 ]. In pregnant mice, infusion of AVP causes hypertension and renal glomerular endotheliosis, issuing placental oxidative stress which alters placental morphology, production of placental growth factor (PGF), and placental gene expression leading to intrauterine growth restriction, all mimicking dysfunctions seen during human pre-eclampsia [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of Stress-Mediating Genes is Increased in Term Placentas of Women with Chronic Self-Perceived Anxiety and Depression

Martínez

Marteinsdóttir

Josefsson

et al. 2020

Genes

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Anxiety, chronical stress, and depression during pregnancy are considered to affect the offspring, presumably through placental dysregulation. We have studied the term placentae of pregnancies clinically monitored with the Beck’s Anxiety Inventory (BAI) and Edinburgh Postnatal Depression Scale (EPDS). A cutoff threshold for BAI/EPDS of 10 classed patients into an Index group (>10, n = 23) and a Control group (<10, n = 23). Cortisol concentrations in hair (HCC) were periodically monitored throughout pregnancy and delivery. Expression differences of main glucocorticoid pathway genes, i.e., corticotropin-releasing hormone (CRH), 11β-hydroxysteroid dehydrogenase (HSD11B2), glucocorticoid receptor (NR3C1), as well as other key stress biomarkers (Arginine Vasopressin, AVP and O-GlcNAc transferase, OGT) were explored in medial placentae using real-time qPCR and Western blotting. Moreover, gene expression changes were considered for their association with HCC, offspring, gender, and birthweight. A significant dysregulation of gene expression for CRH, AVP, and HSD11B2 genes was seen in the Index group, compared to controls, while OGT and NR3C1 expression remained similar between groups. Placental gene expression of the stress-modulating enzyme 11β-hydroxysteroid dehydrogenase (HSD11B2) was related to both hair cortisol levels (Rho = 0.54; p < 0.01) and the sex of the newborn in pregnancies perceived as stressful (Index, p < 0.05). Gene expression of CRH correlated with both AVP (Rho = 0.79; p < 0.001) and HSD11B2 (Rho = 0.45; p < 0.03), and also between AVP with both HSD11B2 (Rho = 0.6; p < 0.005) and NR3C1 (Rho = 0.56; p < 0.03) in the Control group but not in the Index group; suggesting a possible loss of interaction in the mechanisms of action of these genes under stress circumstances during pregnancy.

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Arginine vasopressin infusion is sufficient to model clinical features of preeclampsia in mice

Cited by 61 publications

References 114 publications

Pre-eclampsia: pathogenesis, novel diagnostics and therapies

Pre-eclampsia: pathogenesis, novel diagnostics and therapies

Expression of Stress-Mediating Genes Is Increased in Term Placentas of Women with Chronic Self-Perceived Anxiety and Depression

Expression of Stress-Mediating Genes is Increased in Term Placentas of Women with Chronic Self-Perceived Anxiety and Depression

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