Inhibition of Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Protects against Plasma/Hypoxia-Mediated Trophoblast Dysfunction Associated with Preeclampsia

Zhang, Yan; Ye, Yuanhua; Chen, Weiping

doi:10.1159/000370195

Cited by 11 publications

(3 citation statements)

References 40 publications

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“…However, they found that methylglyoxal, which is involved in vascular complications of diabetes mellitus and the development of hypertension, is a possible factor that affects LOX-1 and arginase because it is able to induce oxidative stress in vascular cells. Another finding by Zhang and colleagues suggests that LOX-1 accumulation may contribute to the development of PE by promoting sFlt-1 production in trophoblasts ( 23 ). This group was able to inhibit LOX-1 and protect against oxidative stress-mediated trophoblast dysfunction.…”

Section: Endothelial Dysfunction Pregnancy and Innate Immunitymentioning

confidence: 99%

Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia

Bounds

Newell‐Rogers

2015

Front. Cardiovasc. Med.

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The maternal innate immune system plays an important role both in normal pregnancy as well as hypertensive disorders of pregnancy including preeclampsia (PE). We propose four pathways that involve excessive innate immunity that lead to most forms of PE. Pre-existing endothelial dysfunction plus pregnancy leads to an excessive innate immune response resulting in widespread inflammation, placental and renal dysfunction, vasoconstriction, and PE. Placental dysfunction due to shallow trophoblast invasion, inadequate spiral artery remodeling, and/or low placental perfusion initiates an innate immune response leading to excessive inflammation, endothelial and renal dysfunction, and PE. A heightened innate immune system due to pre-existing or acquired infections plus the presence of a paternally derived placenta and semi-allogeneic fetus cause an excessive innate immune response which manifests as PE. Lastly, an abnormal and excessive maternal immune response to pregnancy leads to widespread inflammation, organ dysfunction, and PE. We discuss the potential role of innate immunity in each of these scenarios, as well as the overlap, and how targeting the innate immune system might lead to therapies for the treatment of PE.

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Section: Endothelial Dysfunction Pregnancy and Innate Immunitymentioning

confidence: 99%

Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia

Bounds

Newell‐Rogers

2015

Front. Cardiovasc. Med.

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“…The role of oxidative stress in the pathophysiology of PE has increasingly been postulated thus: reactive oxygen species produced by the relatively hypoxic placenta is transferred to the maternal circulation and it subsequently causes endothelial dysfunction [10]. Moreover oxidative stress may be an important mediator regulating angiogenic pathways in trophoblasts [11]. The pathogenesis of PE involves a number of biological processes that may be directly or indirectly affected by vitamin D, including immune dysfunction, placental implantation, pregestational insulin resistance, abnormal angiogenesis, excessive inflammation, and hypertension [12,13,14].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Status Is Related to Oxidative Stress But Not High-Sensitive C-Reactive Protein in Women with Pre-Eclampsia

Gargari

Tabrizi²,

Sadien³

et al. 2015

Gynecol Obstet Invest

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Background/Aims: Pre-eclampsia (PE) is associated with unfavorable metabolic profiles. Oxidative stress and inflammation have been increasingly postulated as major contributors to PE. Research suggests that vitamin D status is disturbed in women with PE. The aims of this study were to compare the serum levels of vitamin D and oxidative stress status in women with PE vs. women with normal pregnancies, and to evaluate the relationship between these 2 factors in women with PE. Methods: In this case-control study, 40 women with PE and 40 healthy pregnant women were selected, and high-sensitivity C-reactive protein, malondialdehyde (MDA), total antioxidant capacity (TAC) and 25-hydroxyvitamin D (25(OH)D) levels were assessed. We compared the biochemical indicators between the 2 groups by analysing the data using the independent t test, Mann-Whitney U test, chi-square and logistic regression. Results: Compared with the controls, the serum levels of MDA in women with PE were significantly higher (p = 0.001) and TAC and 25(OH)D levels were significantly lower (p < 0.05). TAC concentration was positively associated with 25(OH)D levels in cases of PE (β = 0.428, p = 0.01). Conclusion: Our findings show lower levels of TAC and 25(OH)D in women with PE in comparison to controls, while having similar vitamin D intakes. In addition, our results suggest a positive relationship between TAC concentration and 25(OH)D levels in PE cases.

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“…Although the physiopathology associated with preeclampsia (PE) is unclear, oxidative stress appears to be an important contributing factor [1]. Heme oxygenase-1 (HO-1) is an inducible enzyme that catalyzes heme degradation, which triggers the synthesis of iron, biliverdin, and carbon monoxide, resulting in anti-inflammatory and anti-apoptotic effects, and oxidation resistance [2,3].…”

Section: Introductionmentioning

confidence: 99%

Increased Heme Oxygenase-1 and Nuclear Factor Erythroid 2-Related Factor-2 in the Placenta Have a Cooperative Action on Preeclampsia

Zhou

et al. 2016

Gynecol Obstet Invest

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Background: Previous studies have shown that oxidative stress is an important factor in preeclampsia (PE). Heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor-2 (Nrf2) are protective proteins that are involved in combating oxidative stress in the body. Nrf2 is also an essential upstream transcription factor regulating HO-1. This study was aimed at exploring the physiological roles of HO-1 and Nrf2 in PE. Methods: Serum and placenta were collected from 30 patients who presented with severe PE and 30 healthy pregnant females. HO-1 and Nrf2 levels in placenta were measured. Following stimulation of the HTR-8/SVneo cell line with tert-butylhydroquinone (tBHQ), an Nrf2 activator, nuclear Nrf2 protein and HO-1 mRNA levels were determined. Results: Compared with the healthy pregnancy group, HO-1 protein and mRNA levels were increased in placental samples obtained from the severe PE group (p < 0.01, p < 0.05). Similar increases were also observed for Nrf2 protein levels (p < 0.01). Nuclear Nrf2 protein and HO-1 mRNA levels were both increased in the HTR-8/SVneo cell line following stimulation with tBHQ (p < 0.05). Conclusion: Patients with severe PE may be protected against oxidative injury following an elevation in HO-1 and Nrf2 levels. Nrf2 is likely to have a synergistic effect on HO-1 in PE.

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Inhibition of Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Protects against Plasma/Hypoxia-Mediated Trophoblast Dysfunction Associated with Preeclampsia

Cited by 11 publications

References 40 publications

Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia

Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia

Vitamin D Status Is Related to Oxidative Stress But Not High-Sensitive C-Reactive Protein in Women with Pre-Eclampsia

Increased Heme Oxygenase-1 and Nuclear Factor Erythroid 2-Related Factor-2 in the Placenta Have a Cooperative Action on Preeclampsia

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