Relationship between the concentration of ergothioneine in plasma and the likelihood of developing pre-eclampsia.
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SUBMITTER: Kenny LC
PROVIDER: S-EPMC10326187 | biostudies-literature | 2023 Jul
REPOSITORIES: biostudies-literature
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Relationship between the concentration of ergothioneine in plasma and the likelihood of developing pre-eclampsia.
Kenny Louise C LC Brown Leslie W LW Ortea Paloma P Tuytten Robin R Kell Douglas B DB
Bioscience reports 20230701 7
Ergothioneine, an antioxidant nutraceutical mainly at present derived from the dietary intake of mushrooms, has been suggested as a preventive for pre-eclampsia (PE). We analysed early pregnancy samples from a cohort of 432 first time mothers as part of the Screening for Endpoints in Pregnancy (SCOPE, European branch) project to determine the concentration of ergothioneine in their plasma. There was a weak association between the ergothioneine levels and maternal age but none for BMI. Of these 4 ...[more]
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Project description:IntroductionPre-eclampsia is a major cause of maternal and fetal mortality and morbidity worldwide. Its pathophysiology remains unclear, but mitochondrial dysfunction and oxidative stress have been implicated. L-Ergothioneine is a naturally occurring, water-soluble betaine, that has demonstrated antioxidant properties. Using the reduced uterine perfusion pressure (RUPP) rat model of pre-eclampsia, this study aimed to define the plasma metabolic profile following treatment with L-Ergothioneine.MethodsThe effect of L-Ergothioneine (ET) treatment was explored using in vivo treatment in rats: Sham control (SC, n = 5), RUPP control (RC, n = 5), Sham +ET (ST, n = 5), RUPP +ET (RT, n = 5). Differential expression of plasma metabolites were obtained using untargeted liquid chromatography coupled to mass spectrometry. Statistical analysis was performed on normalised data comparing RC to SC, RT to RC, and RT to ST. Metabolites significantly altered (FDR < 0.05) were identified through database search.ResultsWe report significantly lower levels of L-palmitoylcarnitine in RC compared to SC, a fatty acyl substrate involved in beta-oxidation in the mitochondria. We report that a metabolite that has been associated with oxidative stress (Glutamylcysteine) was detected at significantly higher levels in RT vs RC and RT vs ST. Five metabolites associated with inflammation were significantly lower in RT vs RC and three metabolites in RT vs ST, demonstrating the anti-inflammatory effects of ET in the RUPP rat model of pre-eclampsia.ConclusionsL-Ergothioneine may help preserve mitochondrial function by increasing antioxidant levels, and reducing inflammatory responses associated with pre-eclampsia. This study shows the potential of L-Ergothioneine as a treatment for pre-eclampsia.
| S-EPMC7108727 | biostudies-literature
Project description:BackgroundStudies have suggested controversial results regarding a possible association between pre-eclampsia (PE) and periodontal disease (PD) and no meta-analysis has been performed to clarify this issue.MethodsA literature search of electronic databases was performed for articles published through March 24, 2013, followed by a manual search of several dental and medical journals. The meta-analysis was conducted according to the recommendations of the Cochrane Collaboration and PRISMA. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Heterogeneity was assessed with the χ(2)-based Cochran Q test and I(2) statistic. The level of significance was set at P <0.05.ResultsFifteen studies were included, including three cohort and 12 case-control studies. A positive association was found between PE and PD (OR 2.17, 95% CI 1.38-3.41, P = 0.0008). However, a high and significant heterogeneity was found (χ(2) = 62.42, P<0.00001, I(2) = 75%). In most cases, subgroup analysis had low power to detect significant differences between PE and non-PE groups.ConclusionBased on the findings of the meta-analysis, PD appears to be a possible risk factor for PE. However, given the important differences in the definitions and diagnoses of PD and PE among the studies, as well as their lack of good methodological quality, future trials are needed to confirm the results of the present meta-analysis.
| S-EPMC3747173 | biostudies-literature
Project description:ObjectivesThe goal of this study was to systematically review the peripartum cardiomyopathy (PPCM) literature and determine the prevalence of pre-eclampsia (PE) in women with PPCM. Secondary analyses included evaluation of the prevalence of hypertensive disorders, multiple gestations, and multiparity.BackgroundPPCM is a significant cause of maternal and infant morbidity and mortality worldwide, yet its etiology remains unknown. PE is often cited as a risk factor for the development of PPCM and recent research suggests that PE and PPCM share mechanisms that contribute to their pathobiology. No comprehensive evaluation of the relationship between PE and PPCM exists.MethodsA systematic predetermined search strategy was performed in multiple databases to identify studies describing ≥3 women with PPCM. Prevalence rates of PE, hypertension, multiple gestations, and multiparity were pooled.ResultsData from 22 studies (n = 979) were included in this analysis. The pooled prevalence of 22% (95% confidence interval [CI]: 16% to 28%) was more than quadruple the 5% average worldwide background rate of PE in pregnancy (p < 0.001). There were no geographic or racial differences detected in the prevalence of PE in women with PPCM. The rates of hypertension during pregnancy (37% [95% CI: 29% to 45%]) and multiple gestations (9% [95% CI: 7% to 11%]) were also elevated.ConclusionsThe prevalence of PE, hypertensive disorders, and multiple gestations in women with PPCM is markedly higher than that in the general population. These findings support the concept of a shared pathogenesis between PE and PPCM and highlight the need for awareness of the overlap between these 2 diseases.
| S-EPMC3931606 | biostudies-literature
Project description:BackgroundEpidemiological observational studies have investigated the relationship between rheumatoid arthritis(RA) and pre-eclampsia, but no consistent conclusions were obtained due to various limitations. Hence, we conducted a two-sample mendelian randomization analysis to evaluate the potential causal effect of RA on pre-eclampsia.MethodsSummary-level statistics for RA were derived from a large-scale meta-analysis of datasets of genome-wide association studies(GWAS) which involved 14,361 cases and 43,923 controls. Moreover, summary statistics for pre-eclampsia or eclampsia were sourced from the Finn biobank which contained 3,903 cases and 114,735 controls. The inverse variance weighting (IVW) as well as other four effective methods including MR-Egger, weighted median, weighted mode, and simple mode were applied to deduce the potential causal relationships between RA and pre-eclampsia comprehensively.ResultsThe two-sample MR analysis suggested a strong causal relationship between RA and pre-eclampsia[OR,1.05;95%CI, 1.01-1.09;p<0.05]. The OR estimates obtained from the weighted mode[OR,1.09;95%CI,1.03-1.15;p<0.01] and weighted median[OR,1.07;95%CI, 1.01-1.14;p<0.05] were similar to those from the IVW method, but there was no significant association observed in MR Egger and simple mode analysis.ConclusionThis MR analysis provides evidence of a positive causal association between RA and pre-eclampsia genetically. Our findings highlight the importance of more intensive prenatal care and early intervention among pregnant women with RA to prevent potential adverse obstetric outcomes. Moreover, our study provides clues for risk factor identification and early prediction of pre-eclampsia.
| S-EPMC9790901 | biostudies-literature
Project description:Sphingolipids like sphingosine-1-phosphate (S1P) have been implicated in the pathophysiology of pre-eclampsia. We hypothesized that plasma S1P would be increased in women at high risk of developing pre-eclampsia who subsequently develop the disease. Low circulating placental growth factor (PlGF) is known to be associated with development of pre-eclampsia; so further, we hypothesized that increased S1P would be associated with concurrently low PlGF. This was a case-control study using stored maternal blood samples from 14 to 24 weeks of pregnancy, collected from 95 women at increased risk of pre-eclampsia. Pregnancy outcome was classified as uncomplicated, preterm pre-eclampsia (<37 weeks), or term pre-eclampsia. Plasma lipids were extracted and analyzed by ultraperformance liquid chromatography coupled to electrospray ionization MS/MS to determine concentrations of S1P and sphingosine. Median plasma S1P was 0.339 nmol/ml, and median sphingosine was 6.77 nmol/l. There were no differences in the plasma concentrations of S1P or sphingosine in women who subsequently developed pre-eclampsia, no effect of gestational age, fetal sex, ethnicity, or the presence of pre-existing hypertension. There was a correlation between S1P and sphingosine plasma concentration (P < 0.0001). There was no relationship between S1P or sphingosine with PlGF. Previous studies have suggested that plasma S1P may be a biomarker of pre-eclampsia. In our larger study, we failed to demonstrate there are women at high risk of developing the disease. We did not show a relationship with known biomarkers of the disease, suggesting that S1P is unlikely to be a useful predictor of the development of pre-eclampsia later in pregnancy.
| S-EPMC9760648 | biostudies-literature
Project description:OBJECTIVES:To examine the relationship between abnormalities in uterine (UtA) and/or umbilical artery (UA) Doppler velocimetry and maternal plasma concentrations of soluble endoglin (sEng) in patients with pre-eclampsia (PE). METHODS:A cross-sectional study was conducted in 135 normal pregnant women and 69 patients with PE. Patients with PE were subclassified into four groups: those who had Doppler abnormalities in both the UtA and UA, patients who had Doppler abnormalities in the UtA alone, those who had Doppler abnormalities in the UA alone, and patients without Doppler abnormalities in either vessel. Plasma concentrations of sEng were determined by enzyme-linked immunosorbent assay. RESULTS:Among patients with PE, those with abnormal UtA and UA Doppler velocimetry had the highest median plasma concentration of sEng compared with any other group (P < 0.001, Kruskal-Wallis test). Women with PE with normal Doppler velocimetry in both vessels had the lowest median plasma concentration of sEng. There was a significant relationship between plasma concentrations of sEng and mean UtA resistance index (Spearman Rho = 0.5, P < 0.001) as well as UA pulsatility index (Spearman Rho = 0.4, P = 0.002). Multiple regression analysis suggested that Doppler abnormalities in the UtA and UA as well as gestational age at blood sampling contributed to plasma sEng concentrations (P < 0.001). CONCLUSIONS:Abnormalities of impedance to blood flow in the UtA and UA are associated with an excess of sEng in the circulation of mothers with PE. These findings suggest that the 'antiangiogenic state' in PE is partially reflected in abnormalities of Doppler velocimetry.
| S-EPMC2944768 | biostudies-literature
Project description:The etiology of preeclampsia, a hypertensive disorder of human pregnancy, remains unknown. We addressed fetal sex selection and the suggestive role of fetal HLA-G and related genes, regulating maternal immune responses, in preeclampsia pathogenesis. We assessed birth sex ratios, weights, and seasonality of preeclampsia among 1.79 million births in Finland. We studied haplotypes of HLA-G 3’ untranslated region (UTR), regulating HLA-G expression, in 1000 Genomes series and in a preeclampsia cohort (n=1249). We quantified placental (n=163) mRNA expression of 136 genes, studied HLA-G and IFNα protein expression by immunohistochemistry, and measured maternal and fetal circulating IFNα levels by ELISA. Population-level data showed loss of male fetuses as a characteristic of preeclampsia. As a potential contributor to immune-mediated loss, we found balancing selection at HLA-G 3’UTR modulating sex ratio, and association of HLA-G 3’UTR haplotypes with placental HLA-G expression. HLA-G and its receptors were downregulated in preeclampsia placentas, and surprisingly, interferon alpha-1 (IFNA1) was highly upregulated. IFNA1 and HLA-G distinguished preeclampsia better than placental FLT1 expression. Fetal but not maternal circulating IFNα, produced by trophoblasts, showed association with maternal hypertension and fetal growth restriction. We uncover the link between placental HLA-G expression and human birth sex ratio. We propose that preeclampsia shares, through reduced HLA-G mediated immunotolerance, the mechanism needed to fight placental viral infections and malaria in evolution. IFNα upregulation in preeclampsia placenta, together with its known actions upstream of inflammatory genes, encourages testing IFNα inhibitors and especially the pregnancy-approved antimalarial hydroxichloroquine in treatment of preeclampsia.
2019-11-25 | GSE125460 | GEO
Project description:Hypertensive disorders of pregnancy (HDP), comprising gestational hypertension (GH) and pre-eclampsia (PE), are leading causes of maternal and perinatal morbidity and mortality. Both GH and PE are characterized by new-onset hypertension, but PE additionally includes proteinuria and/or end-organ damage. Impaired nitric oxide (NO) bioavailability may lead to endothelial dysfunction in GH and PE, and the primary source of vascular NO is endothelial NO synthase (eNOS). However, no previous study has investigated plasma eNOS concentrations in patients with GH and PE. In this study, we compared plasma eNOS concentrations in healthy pregnancies and HDP in two independent cohorts. The primary study included 417 subjects, with 43 non-pregnant (NP) and 156 healthy pregnant (HP) women and 122 patients with GH and 96 with PE. The replication study included 85 pregnant women (41 healthy and 44 pre-eclamptic). Plasma concentrations of eNOS were measured using a commercial ELISA kit provided by R&D Systems, and plasma nitrite concentrations were assessed using two ozone-based chemiluminescence assays. Correlations between plasma eNOS concentrations and plasma nitrite concentrations, as well as clinical and biochemical parameters, were evaluated by either Spearman's or Pearson's tests. In the primary study, NP women and HDP had significantly lower plasma eNOS concentrations compared to HP; concentrations were even lower in PE compared to GH. Plasma eNOS concentrations were reduced but not significant in early-onset PE, PE with severe features, preterm birth, and intrauterine growth restriction. No correlation was observed between plasma eNOS and nitrite levels. In HDP, there was a significant positive correlation between levels of eNOS and hemoglobin (r = 0.1496, p = 0.0336) as well as newborn weight (r = 0.1487, p = 0.0316). Conversely, a negative correlation between eNOS levels and proteinuria was observed (r = -0.2167, p = 0.0179). The replication study confirmed significantly reduced plasma concentrations of eNOS in PE compared to HP. Our findings provide evidence of reduced plasma eNOS concentrations in HDP; they were particularly lower in PE compared to GH and HP in two independent studies.
| S-EPMC10660730 | biostudies-literature
Project description:Pre-eclampsia (PE) is a chronic inflammatory disease in pregnancy, which is associated with enhanced blood coagulation and high thrombotic risk. To date, the mechanisms underlying such an association are not fully understood. Previous studies reported high levels of plasma deoxyribonucleic acid (DNA) in PE women, but the cellular source of the circulation DNA remains unknown. In this study, we tested the hypothesis that activated neutrophils undergoing cell death, also called NETosis, may be responsible for the elevated plasma DNA levels in PE women. We analysed plasma samples from non-pregnant, normal pregnant and PE women and found high levels of double-stranded DNA, myeloperoxidase (an abundant neutrophil granular enzyme) and histones (the major nucleosome proteins) in PE-derived samples, indicating increased NETosis in the maternal circulation. The high plasma DNA levels positively correlated with enhanced blood coagulation in PE women. When isolated neutrophils from normal individuals were incubated with PE-derived plasma, an elevated NETosis-stimulating activity was detected. Further experiments showed that endothelial micro-particles, but not soluble proteins, in the plasma were primarily responsible for the NETosis-stimulating activity in PE women. These results indicate that circulating micro-particles from damaged maternal endothelium are a potent stimulator for neutrophil activation and NETosis in PE women. Given the pro-coagulant and pro-thrombotic nature of granular and nuclear contents from neutrophils, enhanced systemic NETosis may represent an important mechanism underlying the hyper-coagulability and increased thrombotic risk in PE.
| S-EPMC6567982 | biostudies-literature
Project description:BackgroundPre-eclampsia is the most common complication occurring during pregnancy. In the majority of cases, it is concurrent with other pathologies in a comorbid manner (frequent co-occurrences in patients), such as diabetes mellitus, gestational diabetes and obesity. Providing bronchial asthma, pulmonary tuberculosis, certain neurodegenerative diseases and cancers as examples, we have shown previously that pairs of inversely comorbid pathologies (rare co-occurrences in patients) are more closely related to each other at the molecular genetic level compared with randomly generated pairs of diseases. Data in the literature concerning the causes of pre-eclampsia are abundant. However, the key mechanisms triggering this disease that are initiated by other pathological processes are thus far unknown. The aim of this work was to analyse the characteristic features of genetic networks that describe interactions between comorbid diseases, using pre-eclampsia as a case in point.ResultsThe use of ANDSystem, Pathway Studio and STRING computer tools based on text-mining and database-mining approaches allowed us to reconstruct associative networks, representing molecular genetic interactions between genes, associated concurrently with comorbid disease pairs, including pre-eclampsia, diabetes mellitus, gestational diabetes and obesity. It was found that these associative networks statistically differed in the number of genes and interactions between them from those built for randomly chosen pairs of diseases. The associative network connecting all four diseases was composed of 16 genes (PLAT, ADIPOQ, ADRB3, LEPR, HP, TGFB1, TNFA, INS, CRP, CSRP1, IGFBP1, MBL2, ACE, ESR1, SHBG, ADA). Such an analysis allowed us to reveal differential gene risk factors for these diseases, and to propose certain, most probable, theoretical mechanisms of pre-eclampsia development in pregnant women. The mechanisms may include the following pathways: [TGFB1 or TNFA]-[IL1B]-[pre-eclampsia]; [TNFA or INS]-[NOS3]-[pre-eclampsia]; [INS]-[HSPA4 or CLU]-[pre-eclampsia]; [ACE]-[MTHFR]-[pre-eclampsia].ConclusionsFor pre-eclampsia, diabetes mellitus, gestational diabetes and obesity, we showed that the size and connectivity of the associative molecular genetic networks, which describe interactions between comorbid diseases, statistically exceeded the size and connectivity of those built for randomly chosen pairs of diseases. Recently, we have shown a similar result for inversely comorbid diseases. This suggests that comorbid and inversely comorbid diseases have common features concerning structural organization of associative molecular genetic networks.
| S-EPMC4407242 | biostudies-literature