Preeclampsia

Ramos, José Geraldo Lopes; Sass, Nelson; Costa, Sérgio Ely Valadão Gigante de Andrade

doi:10.1055/s-0037-1604471

Cited by 143 publications

(110 citation statements)

References 77 publications

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“…A previous study reported that E2 suppressed the binding activity of NF-κB mediated by ERα66 and reduced the expression of MMP2, MMP9, cyclin A and cyclin d1, resulting in cell cycle arrest and promoting cell apoptosis (36). Apoptotic processes and endothelial dysfunction are common in PE (3). The results of the present study indicated that that E2 suppressed the expression of MMP9, MMP2 and VcAM-1 in placental tissue induced by L-NAME treatment.…”

Section: Discussionsupporting

confidence: 54%

“…It is the major cause of maternal and perinatal death, premature birth and fetal growth restriction; the pathogenesis is complex and effective treatments are currently lacking (1,2). PE is a chronic disease, which frequently leads to multiple organ failure in the body of the pregnant woman, increases the production of reactive oxygen species, causes maternal inflammation and accelerates apoptosis, leading to an imbalance between the formation of normal placentation and pro-angiogenic factors (3). Previous studies have demonstrated that compared with non-pregnant females, those with normal pregnancy and patients with PE exhibit an inflammatory response, and that patients with PE exhibit excessive activation of the inflammatory response compared with normal pregnant subjects, including increased levels of inflammatory cytokines and products of oxidative stress (4,5).…”

Section: Introductionmentioning

confidence: 99%

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The effects of estradiol on inflammatory and endothelial dysfunction in rats with preeclampsia

Lin¹,

Jin²,

Shan³

2020

Int J Mol Med

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Preeclampsia (PE), a hypertensive disorder during pregnancy, has adverse effects to both the mother and the fetus. Maternal inflammatory and vascular endothelial dysfunction are important factors in the pathogenesis of PE. The present study aimed to investigate the effects of estradiol (E2) on inflammatory and endothelial dysfunction in an N (omega)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE. Adult pregnant female Sprague-dawley rats were divided into four equal groups between days 7 and 11 of gestation and treated as follows: i) Pregnant rats receiving daily intraperitoneal (i.p.) injections of equal volume of 0.9% normal saline (NS) (control group, n=12); ii) pregnant rats receiving daily i.p. injections of L-NAME at 50 mg/kg (L-NAME group, n=12); iii) pregnant rats receiving a daily i.p. injection of 50 mg/kg L-NAME and NS from day 11 (L-NAME + NS group, n=12); and iv) pregnant rats receiving daily i.p. injections of 50 mg/kg L-NAME and 100 µg/kg/day E2 from day 11 (L-NAME + E2 group, n=12). On day 21, blood pressure (BP) and the level of 24-h urine protein in the maternal rats, fetal weight and percentage of stillbirths following a cesarean section were recorded. The activities of nitric oxide (NO) and inducible NO synthase (iNOS), the levels of inflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ and monocyte chemoattractant protein-1], adherence factors (cd49d, intracellular adhesion molecule 1 and lymphocyte function-associated antigen-1) and uterine angiogenic status (Fms-like tyrosine kinase-1, vascular cell adhesion molecule and matrix metalloproteinase 2/9) were also assessed. In addition, the histopathology of the placenta, the expression of estrogen receptor α 36 (ERα36), ERα, ERβ and G protein-coupled ER, as well as the activation of the toll-like receptor 4 (TLR4) signaling pathway (TLR4, myeloid differentiation primary response 88, IL-1 receptor-associated kinase 4 and tumor necrosis factor receptor-associated factor 6) were evaluated by H&E staining, immunofluorescence and western blot assays. Treatment with L-NAME increased the BP, urine protein and rate of stillbirths and suppressed fetal weight compared with those in the control group. The L-NAME-induced effects were attenuated by the administration of E2. In addition, the administration of E2 decreased inflammation and NO levels and altered the uterine angiogenic status. The histological analysis of PE rat placenta in the E2-treated group confirmed the effects on biochemical parameters. Of note, E2 treatment significantly suppressed the TLR4 signaling pathway. In the rat model of PE, adverse outcomes including BP, fetal rat weight and proteinuria, high neonatal death rate, inflammatory response, oxidative stress and endothelial dysfunction were attenuated by exogenous E2 administration, which may present a novel approach for the clinical treatment of PE.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

The effects of estradiol on inflammatory and endothelial dysfunction in rats with preeclampsia

Lin¹,

Jin²,

Shan³

2020

Int J Mol Med

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“…It can be accompanied by abnormal changes in the heart, lung, liver, kidney, and other vital organs or the blood system, digestive system, nervous system, and placenta-fetal interface, and thus is a major cause of morbidity and mortality in maternal and fetal medicine [2,3]. The incidence of PE is estimated to be 3-5% of pregnancies worldwide [4], but 8.1% in developing countries, which the mortality rate for mothers can reach 22.0% [5]. The clinical symptoms of PE are reflected in three aspects; the first involves placental perfusion dysfunction followed by a systemic inflammatory response, the second is vascular endothelial damage, and the last is oxidative stress [1].…”

Section: Introductionmentioning

confidence: 99%

Haplotype Analysis of Candidate Genes Involved in Inflammation and Oxidative Stress and the Susceptibility to Preeclampsia

Chen

Zhao

Wang

et al. 2020

Journal of Immunology Research

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Unbalanced inflammatory reactions and oxidative stress are inseparably interconnected, and both may play crucial roles in the pathophysiological mechanisms of preeclampsia (PE). In the published previous studies, we have genotyped for SNPs that related to inflammation (rs2227485, rs153109, rs17855750, rs2027432, rs2275913, rs763780, rs4819554, and rs13015714) and oxidative stress (rs1695, rs4680, rs1800566, rs4807542, rs713041, rs7579, rs230813, rs1004467, rs3824755, and rs9932581) to investigate whether these polymorphisms were associated with susceptibility to PE in a Chinese Han population. In this present study, we collected these data of experimental and clinical from above studies for haplotype analysis of inflammation-related SNPs in 631 PE patients and 720 normal pregnancy and oxidative stress-related SNPs in 342 PE patients and 457 normal pregnancies for susceptibility to PE. The data of genotype distribution and allele frequency comparisons after correction for multiple comparisons (P/8 or P/10) showed 2 among the 8 candidate inflammation-related SNPs have significant differences (rs2027432 genotype χ2=407.377,p<0.001,p<0.00625). Moreover, the minor alleles of rs2027432 T (minor allele χ2=450.923,p<0.001,p<0.00625;OR=21.439,95%CI=15.181‐30.278) and rs4819554 G (minor allele χ2=163.465,p<0.001,p<0.00625;OR=5.814,95%CI=4.380‐7.719) were confirmed as risk allele of PE, respectively. Our analysis revealed rs2027432 (TT) of NLRP3 and rs4819554 (GG) of IL-17RA are risk factors for PE. However, no significant difference was found at the oxidative stress-related SNPs. In the candidate loci for oxidative stress, we also identified 3 SNP matches (rs4807542 and rs713041, rs230813 and rs75799, rs1004467 and rs3824755) that had high linkage disequilibrium (LD) with each other and were selected as a block (r2=0.98,r2=0.97,r2=0.97,r2>0.9), and the GT and GC haplotypes of rs4807542 and rs713041 in GPX4 showed significant differences between the PE and control groups (χ2=5.143,p=0.0233,p<0.05;χ2=6.373,p=0.0116,p<0.05). So, we inferred that polymorphisms of NLRP3 rs2027432 and IL-17RA rs4819554, which are related to inflammation, and the rs713041 variant of GPX4, which is related to oxidative stress, were associated with susceptibility to PE. The GT and GC haplotypes of rs4807542 and rs713041 in GPX4 may increase the risk of PE in the Chinese Han population.

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“…Preeclampsia is defined as a multisystemic disease characterized by a combination of elevated blood pressure (systolic BP ≥140 mmHg or diastolic BP ≥ 90 mmHg), first identified after 20 weeks of gestation, and proteinuria, and may coincide with another hypertensive state (4) .…”

Section: Introductionmentioning

confidence: 99%

Maternal characteristics and risk factors for preeclampsia in pregnant women

Ferreira¹,

Moura²,

Gomes³

et al. 2019

Rev Rene

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Objective: to investigate maternal characteristics and risk factors for development of preeclampsia in pregnant women. Methods: documentary and retrospective study based on medical records of pregnant women of six Family Health Strategy teams. Information of 94 pregnant women was collected through a form and used in the study. Results: the pregnant women were aged between 15 and 47 years. The risk factors for development of preeclampsia in the sample were primiparity 40 (42.6%), chronic hypertension 4 (4.3%), multiple pregnancy 9 (9.6%), diabetes mellitus and obesity 8 (8.6%), and age >40 years (1.1%). Conclusion: there were some risk factors for the development of preeclampsia in the evaluated registries, such as primiparity, chronic hypertension, diabetes mellitus and obesity. Descriptors: Risk Factors; Pre-Eclampsia; Prenatal Care; Pregnancy, High-Risk.Objetivo: investigar as características maternas e os fatores de risco para o desenvolvimento da pré-eclâmpsia em gestantes. Métodos: estudo documental e retrospectivo, conduzido em fichas de cadastro de gestantes de seis equipes da Estratégia Saúde da Família. Foram utilizadas as informações de 94 gestantes, sendo esses dados coletados por meio de um formulário. Resultados: as gestantes possuíam idade entre 15 e 47 anos. Os fatores de risco para o desenvolvimento de pré-eclâmpsia presentes na amostra foram a primiparidade 40 (42,6%), a hipertensão crônica 4 (4,3%), a gravidez múltipla 9 (9,6%), o diabetes mellitus e a obesidade 8 (8,6%) e a idade >40 anos (1,1%). Conclusão: houve a presença de alguns fatores de risco para o desenvolvimento da pré-eclâmpsia nos cadastros avaliados, como primiparidade, hipertensão crônica, diabetes mellitus e obesidade.

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Preeclampsia

Cited by 143 publications

References 77 publications

The effects of estradiol on inflammatory and endothelial dysfunction in rats with preeclampsia

The effects of estradiol on inflammatory and endothelial dysfunction in rats with preeclampsia

Haplotype Analysis of Candidate Genes Involved in Inflammation and Oxidative Stress and the Susceptibility to Preeclampsia

Maternal characteristics and risk factors for preeclampsia in pregnant women

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