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pre-eclampsia/protease
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Proteases Activate Pregnancy Neutrophils by a Protease-Activated Receptor 1 Pathway: Epigenetic Implications for Preeclampsia
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We tested a novel hypothesis that elevated levels of proteases in the maternal circulation of preeclamptic women activate neutrophils due to their pregnancy-specific expression of protease-activated receptor 1 (PAR-1). Plasma was collected longitudinally from normal pregnant and preeclamptic women
Elevated plasma chymotrypsin-like protease (chymase) activity in women with preeclampsia.
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OBJECTIVE
Chymase, a chymotrypsin-like protease, is a non-ACE angiotensin II (Ang II) generating enzyme. We determined if maternal chymotrypsin-like protease/chymase activity was increased in women with preeclampsia (PE).
METHODS
Maternal plasma was extracted from venous blood of healthy nonpregnant
Effects of placental proteases on maternal and fetal blood pressure in normal pregnancy and preeclampsia.
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Although many protease exist in human placenta, their physiologic roles are still unknown. Our study showed that placenta proteases metabolize vasoactive peptides possibly derived from the fetus. Because vasopressin and angiotensin are known to play an important role in normal and aberrant
Placenta-derived chymotrypsin-like protease (CLP) disturbs endothelial junctional structure in preeclampsia.
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Placenta-derived chymotrypsin-like protease may contribute to endothelial activation in preeclampsia. In this study, we determined if placenta-derived chymotrypsin-like protease could disturb endothelial junctional integrity to promote endothelial permeability in preeclampsia. Confluent endothelial
Increased chymotrypsin-like protease (chymase) expression and activity in placentas from women with preeclampsia.
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Placenta-derived chymotrypsin-like protease (CLP/chymase) promotes endothelial P-selectin and E-selectin expression, which may be responsible for the increased neutrophil/endothelial interactions in preeclampsia (PE). However, little is known about this protease expression and production in human
PAR-2 triggers placenta-derived protease-induced altered VE-cadherin reorganization at endothelial junctions in preeclampsia.
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PAR-2 is a G-protein coupled protease receptor whose activation in endothelial cells (ECs) is associated with increased solute permeability. VE-cadherin is an endothelial-specific junction protein, which exhibits a disorganized distribution at cell junction during inflammation and is a useful
Complement activation, circulating protease inhibitors and pregnancy-associated proteins in severe pre-eclampsia.
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Circulating protease inhibitors, pregnancy-associated proteins and the split product of complement factor 3 (C3d) were measured in 14 women with severe pre-eclampsia and their matched controls. Only the mean levels of antithrombin III were observed to be significantly lower in pre-eclampsia (P less
Altered levels of insulin-like growth factor binding protein proteases in preeclampsia and intrauterine growth restriction.
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Intrauterine growth restriction (IUGR) and preeclampsia (PE) are leading causes of perinatal and maternal morbidity and mortality. Many studies have found association between low levels of insulin-like growth factor binding protein (IGFBP) proteases in the first trimester maternal circulation and
Increased plasma von Willebrand factor antigen levels but normal von Willebrand factor cleaving protease (ADAMTS13) activity in preeclampsia.
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The activity of ADAMTS13, the von Willebrand factor (VWF) cleaving protease is low in several conditions, including HELLP (haemolysis, elevated liver enzymes, and low platelet count) syndrome. As HELLP syndrome develops in most cases on the basis of preeclampsia, our aim was to determine whether
Expressional and epigenetic alterations of placental serine protease inhibitors: SERPINA3 is a potential marker of preeclampsia.
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Preeclampsia is the major pregnancy-induced hypertensive disorder. It modifies the expression profile of placental genes, including several serine protease inhibitors (SERPINs). The objective of this study was to perform a systematic expression analysis of these genes in normal and pathological
Role of proteases in dysfunctional placental vascular remodelling in preeclampsia.
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Preeclampsia is a syndrome characterised by vascular dysfunction, impaired angiogenesis, and hypertension during pregnancy. Even when the precise pathophysiology of preeclampsia remains elusive, impaired vascular remodelling and placental angiogenesis in the placental villi and defective trophoblast
Elevated expression of serine protease HtrA1 in preeclampsia and its role in trophoblast cell migration and invasion.
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OBJECTIVE
Aberrant expression of developmentally regulated genes during placental development could affect fetal growth and contribute to preeclampsia. Expression of serine protease HtrA1 is developmentally regulated with the highest expression in decidua capsularis, compared with ectoplacental
Elevated protease HtrA4 in the maternal circulation of preeclampsia may contribute to endothelial barrier disruption by cleaving key junctional protein VE-cadherin.
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Preeclampsia is hallmarked by systemic endothelial dysfunction, including increased endothelial permeability and oedema. Placenta-derived factors in maternal blood contribute to endothelial barrier impairment, but molecular mechanisms are unclear. HtrA4 is a placenta-specific protease that is
Expression patterns of two serine protease HtrA1 forms in human placentas complicated by preeclampsia with and without intrauterine growth restriction.
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Preeclampsia (PE) and intrauterine growth restriction (IUGR) are pregnancy-specific disorders that have in common abnormal placental implantation, a marked proliferation of villous cytotrophoblastic cells and focal necrosis of the syncytiotrophoblast. Several studies show an ischemic placenta with a
Altered protease expression by periarterial trophoblast cells in severe early-onset preeclampsia with IUGR.
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Adaptation of uteroplacental arteries in patients with early-onset preeclampsia combined with IUGR is compromised due to insufficient invasion of extravillous trophoblast cells (EVT) into the spiral artery wall. The underlying molecular mechanisms are widely unknown. We investigated expression and
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