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Role of lectin-like oxidized low density lipoprotein-1 in fetoplacental vascular dysfunction in preeclampsia.

Zuniga FA, Ormazabal V, Gutierrez N, Aguilera V, Radojkovic C, Veas C, Escudero C, Lamperti L, Aguayo C - Biomed Res Int (2014)

Bottom Line: Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells.However, the role of this receptor in placental tissue is still unknown.In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepción, 4070386 Concepcion, Chile.

ABSTRACT
The bioavailability of nitric oxide (NO) represents a key marker in vascular health. A decrease in NO induces a pathological condition denominated endothelial dysfunction, syndrome observed in different pathologies, such as obesity, diabetes, kidney disease, cardiovascular disease, and preeclampsia (PE). PE is one of the major risks for maternal death and fetal loss. Recent studies suggest that the placenta of pregnant women with PE express high levels of lectin-like oxidized LDL receptor-1 (LOX-1), which induces endothelial dysfunction by increasing reactive oxygen species (ROS) and decreasing intracellular NO. Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells. However, the role of this receptor in placental tissue is still unknown. In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.

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Preeclampsia and LOX-1. In a normal pregnancy adequate trophoblast invasion produces spiral arteries in saccular without a muscular layer, whereby the placental bed is a set of high flow and low resistance. However, in preeclampsia the uteroplacental blood flow was reduced due to an incomplete trophoblast invasion that generates a high strength and low blood flow. Under this condition, placentation arterial lesions were subsequently produced inducing an inflammatory condition, thus increasing perfusion deficit and oxidative stress. In normal pregnancy, lower levels of LOX-1 were found expressed in cells that are part of the trophoblast and syncytiotrophoblast. On the other hand, in preeclampsia LOX-1 levels increase significantly, which may be responsible for the generation of high levels of ROS and decreased levels of NO.
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fig2: Preeclampsia and LOX-1. In a normal pregnancy adequate trophoblast invasion produces spiral arteries in saccular without a muscular layer, whereby the placental bed is a set of high flow and low resistance. However, in preeclampsia the uteroplacental blood flow was reduced due to an incomplete trophoblast invasion that generates a high strength and low blood flow. Under this condition, placentation arterial lesions were subsequently produced inducing an inflammatory condition, thus increasing perfusion deficit and oxidative stress. In normal pregnancy, lower levels of LOX-1 were found expressed in cells that are part of the trophoblast and syncytiotrophoblast. On the other hand, in preeclampsia LOX-1 levels increase significantly, which may be responsible for the generation of high levels of ROS and decreased levels of NO.

Mentions: Although endothelial dysfunction is well described in preeclampsia, the underling mechanism behind this alteration is not completely understood. Several studies have described the release of harmful molecules that may cause endothelial damage from the placenta toward maternal circulation during this disease [104–110]. For instance, the release of soluble receptor type 1 of vascular endothelial growth factor (sFlt-1) [88, 111], soluble endoglin [112], and lipid peroxides [113] has been described. Nowadays, many groups believe that trophoblastic microparticles/nanoparticles shedding toward maternal circulation are a keystone event in the generation of preeclampsia. The investigation is focused on trying to understand how these particles are generated, what would be their content, and what they are doing in the maternal physiology. Actual beliefs explain that incomplete or absent trophoblastic invasion to the uterine spiral arteries is related to reduced uteroplacental blood flow and placental ischemia [83, 105, 114, 115] (see Figure 2). In this scenario, hypoxia/reoxygenation of placental tissue leads to synthesis of free radicals [116] and in particular synthesis and release of reactive oxygen species (ROS), such as superoxide anion, which easily reach the maternal circulation directly or via modification of macromolecules where it can react with NO leading to reduction of NO bioavailability and impaired vascular response [117].


Role of lectin-like oxidized low density lipoprotein-1 in fetoplacental vascular dysfunction in preeclampsia.

Zuniga FA, Ormazabal V, Gutierrez N, Aguilera V, Radojkovic C, Veas C, Escudero C, Lamperti L, Aguayo C - Biomed Res Int (2014)

Preeclampsia and LOX-1. In a normal pregnancy adequate trophoblast invasion produces spiral arteries in saccular without a muscular layer, whereby the placental bed is a set of high flow and low resistance. However, in preeclampsia the uteroplacental blood flow was reduced due to an incomplete trophoblast invasion that generates a high strength and low blood flow. Under this condition, placentation arterial lesions were subsequently produced inducing an inflammatory condition, thus increasing perfusion deficit and oxidative stress. In normal pregnancy, lower levels of LOX-1 were found expressed in cells that are part of the trophoblast and syncytiotrophoblast. On the other hand, in preeclampsia LOX-1 levels increase significantly, which may be responsible for the generation of high levels of ROS and decreased levels of NO.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4109675&req=5

fig2: Preeclampsia and LOX-1. In a normal pregnancy adequate trophoblast invasion produces spiral arteries in saccular without a muscular layer, whereby the placental bed is a set of high flow and low resistance. However, in preeclampsia the uteroplacental blood flow was reduced due to an incomplete trophoblast invasion that generates a high strength and low blood flow. Under this condition, placentation arterial lesions were subsequently produced inducing an inflammatory condition, thus increasing perfusion deficit and oxidative stress. In normal pregnancy, lower levels of LOX-1 were found expressed in cells that are part of the trophoblast and syncytiotrophoblast. On the other hand, in preeclampsia LOX-1 levels increase significantly, which may be responsible for the generation of high levels of ROS and decreased levels of NO.
Mentions: Although endothelial dysfunction is well described in preeclampsia, the underling mechanism behind this alteration is not completely understood. Several studies have described the release of harmful molecules that may cause endothelial damage from the placenta toward maternal circulation during this disease [104–110]. For instance, the release of soluble receptor type 1 of vascular endothelial growth factor (sFlt-1) [88, 111], soluble endoglin [112], and lipid peroxides [113] has been described. Nowadays, many groups believe that trophoblastic microparticles/nanoparticles shedding toward maternal circulation are a keystone event in the generation of preeclampsia. The investigation is focused on trying to understand how these particles are generated, what would be their content, and what they are doing in the maternal physiology. Actual beliefs explain that incomplete or absent trophoblastic invasion to the uterine spiral arteries is related to reduced uteroplacental blood flow and placental ischemia [83, 105, 114, 115] (see Figure 2). In this scenario, hypoxia/reoxygenation of placental tissue leads to synthesis of free radicals [116] and in particular synthesis and release of reactive oxygen species (ROS), such as superoxide anion, which easily reach the maternal circulation directly or via modification of macromolecules where it can react with NO leading to reduction of NO bioavailability and impaired vascular response [117].

Bottom Line: Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells.However, the role of this receptor in placental tissue is still unknown.In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepción, 4070386 Concepcion, Chile.

ABSTRACT
The bioavailability of nitric oxide (NO) represents a key marker in vascular health. A decrease in NO induces a pathological condition denominated endothelial dysfunction, syndrome observed in different pathologies, such as obesity, diabetes, kidney disease, cardiovascular disease, and preeclampsia (PE). PE is one of the major risks for maternal death and fetal loss. Recent studies suggest that the placenta of pregnant women with PE express high levels of lectin-like oxidized LDL receptor-1 (LOX-1), which induces endothelial dysfunction by increasing reactive oxygen species (ROS) and decreasing intracellular NO. Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells. However, the role of this receptor in placental tissue is still unknown. In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.

Show MeSH
Related in: MedlinePlus