Aberrant corin and PCSK6 in placentas of the maternal hyperinsulinemia IUGR rat model

Abassi, Zaid; Kinaneh, Safa; Skarzinski, Galina; Cinnamon, Einat; Smith, Yoav; Bursztyn, Michael; Ariel, Ilana

doi:10.1016/j.preghy.2020.05.007

Cited by 6 publications

(6 citation statements)

References 26 publications

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“…The placenta is another site for corin and pro-ANP expression, indicating a role of ANP in trophoblast function [15,108,109]. In supporting this hypothesis, the ANP receptor NPR-A is expressed in human trophoblasts and decidual stromal cells [16,71].…”

Section: Trophoblast Invasionmentioning

confidence: 86%

“…In addition to the heart, corin is expressed in the placenta [108,109]. In principle, the phenotype in Corin KO mice could result from deficiencies in maternal or fetal corin or both.…”

Section: Corin Ko Micementioning

confidence: 99%

“…In mice, Pcsk6 deficiency prevents corin activation, leading to salt-sensitive hypertension [112]. In a rat model of pregnancy-induced hypertension associated with hyperinsulinemia, reduced corin and PCSK6 expression was found in the placenta [108]. On the other hand, increased PCSK6 expression was reported in placental samples from preeclamptic patients [113].…”

Section: Corin Ko Micementioning

confidence: 99%

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Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia

2023

IJMS

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Endometrial decidualization is a uterine process essential for spiral artery remodeling, embryo implantation, and trophoblast invasion. Defects in endometrial decidualization and spiral artery remodeling are important contributing factors in preeclampsia, a major disorder in pregnancy. Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates blood volume and pressure. ANP is also generated in non-cardiac tissues, such as the uterus and placenta. In recent human genome-wide association studies, multiple loci with genes involved in natriuretic peptide signaling are associated with gestational hypertension and preeclampsia. In cellular experiments and mouse models, uterine ANP has been shown to stimulate endometrial decidualization, increase TNF-related apoptosis-inducing ligand expression and secretion, and enhance apoptosis in arterial smooth muscle cells and endothelial cells. In placental trophoblasts, ANP stimulates adenosine 5′-monophosphate-activated protein kinase and the mammalian target of rapamycin complex 1 signaling, leading to autophagy inhibition and protein kinase N3 upregulation, thereby increasing trophoblast invasiveness. ANP deficiency impairs endometrial decidualization and spiral artery remodeling, causing a preeclampsia-like phenotype in mice. These findings indicate the importance of natriuretic peptide signaling in pregnancy. This review discusses the role of ANP in uterine biology and potential implications of impaired ANP signaling in preeclampsia.

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Section: Trophoblast Invasionmentioning

confidence: 86%

“…In addition to the heart, corin is expressed in the placenta [108,109]. In principle, the phenotype in Corin KO mice could result from deficiencies in maternal or fetal corin or both.…”

Section: Corin Ko Micementioning

confidence: 99%

Section: Corin Ko Micementioning

confidence: 99%

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Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia

2023

IJMS

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“…To date, defective CORIN variants have been found in patients with preeclampsia [9,35,92]. Altered uterine and placental corin expression and shedding have also been reported in animal models and pregnant women with hypertension [9,[93][94][95][96]. Moreover, increased plasma or serum corin levels are found in preeclamptic patients [9,[97][98][99][100][101][102][103].…”

Section: Mechanisms In Uterine Spiral Artery Remodelingmentioning

confidence: 99%

Corin: A Key Mediator in Sodium Homeostasis, Vascular Remodeling, and Heart Failure

Zhang

et al. 2022

Biology

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Atrial natriuretic peptide (ANP) is a crucial element of the cardiac endocrine function that promotes natriuresis, diuresis, and vasodilation, thereby protecting normal blood pressure and cardiac function. Corin is a type II transmembrane serine protease that is highly expressed in the heart, where it converts the ANP precursor to mature ANP. Corin deficiency prevents ANP activation and causes hypertension and heart disease. In addition to the heart, corin is expressed in other tissues, including those of the kidney, skin, and uterus, where corin-mediated ANP production and signaling act locally to promote sodium excretion and vascular remodeling. These results indicate that corin and ANP function in many tissues via endocrine and autocrine mechanisms. In heart failure patients, impaired natriuretic peptide processing is a common pathological mechanism that contributes to sodium and body fluid retention. In this review, we discuss most recent findings regarding the role of corin in non-cardiac tissues, including the kidney and skin, in regulating sodium homeostasis and body fluid excretion. Moreover, we describe the molecular mechanisms underlying corin and ANP function in supporting orderly cellular events in uterine spiral artery remodeling. Finally, we assess the potential of corin-based approaches to enhance natriuretic peptide production and activity as a treatment of heart failure.

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“…Additionally, pregnant mice deficient in corin or ANP have delayed trophoblast invasion, increased blood pressure, and proteinuria, characteristic of preeclampsia [ 27 ], as well as cardiac phenotypes [ 34 ]. Rats with pregnancy-induced hypertension have reduced placental corin, coinciding with fetal growth restriction [ 35 ]. This preeclampsia-like phenotype persists in uterine-specific corin knockout mice that retain cardiac corin expression.…”

Section: Introductionmentioning

confidence: 99%

Investigating the Effects of Atrial Natriuretic Peptide on the Maternal Endothelium to Determine Potential Implications for Preeclampsia

Binder

Beard

Alwis

et al. 2023

IJMS

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Preeclampsia is associated with an increased lifelong risk of cardiovascular disease (CVD). It is not clear whether this is induced by persistent systemic organ and vascular damage following preeclampsia or due to a predisposition to both conditions that share cardiovascular pathophysiology. Common to both CVD and preeclampsia is the dysregulation of corin and its proteolytic product, atrial natriuretic peptide (ANP). ANP, a hypotensive hormone converted from pro-ANP by corin, is involved in blood pressure homeostasis. While corin is predominantly a cardiac enzyme, both corin and pro-ANP are significantly upregulated in the gravid uterus and dysregulated in preeclampsia. Relatively little is known about ANP function in the endothelium during a pregnancy complicated by preeclampsia. Here, we investigated the effect of ANP on endothelial cell proliferation and migration, markers of endothelial dysfunction, and receptor expression in omental arteries exposed to circulating preeclamptic toxins. ANP receptor expression is significantly upregulated in preeclamptic vasculature but not because of exposure to preeclampsia toxins tumour necrosis factor α or soluble fms-like tyrosine kinase-1. The supplementation of endothelial cells with ANP did not promote proliferation or migration, nor did ANP improve markers of endothelial dysfunction. The role of ANP in preeclampsia is unlikely to be via endothelial pathways.

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Aberrant corin and PCSK6 in placentas of the maternal hyperinsulinemia IUGR rat model

Cited by 6 publications

References 26 publications

Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia

Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia

Corin: A Key Mediator in Sodium Homeostasis, Vascular Remodeling, and Heart Failure

Investigating the Effects of Atrial Natriuretic Peptide on the Maternal Endothelium to Determine Potential Implications for Preeclampsia

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