Comparative Transcriptome Analysis of Peripheral Blood in High-Risk Preeclampsia versus Normotensive Pregnancies
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE296973 | GEO | 2025/12/30
REPOSITORIES: GEO
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Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia. Thirty-eight women were included in the study: 19 patients with PE, including 6 women with non-severe PE and 13 with severe PE, and 19 women with normal pregnancy (NP) selected according to age, weight, smoking status, race, gestational age at the inclusion, and blood pH (Table 1 of manuscript). Women with NP had no history of medical illness or medication, and received routing prenatal care. The diagnostic of PE was based on a blood pressure of M-bM-^IM-% 140/90 mmHg taken twice, uricemia above normal laboratory range (120-420 M-BM-5mol/L), and proteinuria higher than 300 mg in a 24 hour-collection, occurring after 20 gestational weeks in previously normotensive women (Table 2). The criteria used to define severe PE included one of the following conditions: a blood pressure higher than 160/110 mmHg, a proteinuria higher than 1500 mg/24h), a multisystem disorder, maternal cerebral symptoms (seizures, stroke) or intrauterine growth restriction below the 3M-BM-0 percentile. Women with multiple gestations, fetal congenital malformations/chromosomal abnormalities, recent infection, antiphospholipid antibodies, trauma, drug or alcohol abuse during pregnancy, preexisting hypertension, thrombophilia with PE history, or women receiving anticoagulant or antiaggregation therapy were excluded from the study. Two microarrays (one non-severe PE and one normal) were discarded from the analysis for technical reasons. Thus, only 36 microarrays are included here.
2014-05-14 | E-GEOD-48424 | biostudies-arrayexpress
Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia.
2014-05-14 | GSE48424 | GEO
Project description:Genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to find differentially expressed genes/pathways. Preeclampsia (PE) is a common and serious pregnancy hypertensive disorder with a strong genetic component. The study aims were to use genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to identify differentially expressed biological pathways, and to determine common pathways between the transcriptome and previously identified maternal susceptibility genes.
2015-08-05 | GSE60438 | GEO
Project description:Genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to find differentially expressed genes/pathways. Preeclampsia (PE) is a common and serious pregnancy hypertensive disorder with a strong genetic component. The study aims were to use genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to identify differentially expressed biological pathways, and to determine common pathways between the transcriptome and previously identified maternal susceptibility genes. Total RNA from decidua basalis obtained from pre-eclamptic and normotensive control patients at Caesarean section
2015-08-05 | E-GEOD-60438 | biostudies-arrayexpress
Project description:Hypertension in pregnancy is the leading cause of morbidity and mortality in pregnancy, affecting up to 10% of all gestations1. Hypertensive disorders of pregnancy include chronic hypertension, gestational hypertension, eclampsia and pre-eclampsia, all of which increase the risk of complications in both mothers and babies during gestation. Preeclampsia, in particular, is characterised by the new-onset of gestational hypertension in the presence of proteinuria or other organ damage. It affects 5-7% of pregnancies and causes approximately 76,000 maternal deaths and 500,000 foetal deaths worldwide each year2. The classification of preeclampsia has been evolving over the last decade. In 2013, American College of Obstetricians and Gynecologists (ACOG) and International Society for the Study of Hypertension in Pregnancy (ISSHP) in the absence of proteinuria included other symptoms/features including liver dysfunction, thrombocytopenia, cerebrovascular events or foetal growth restriction (FGR) in the diagnosis of preeclampsia 1,3,4. Despite the fact that preeclampsia is a multifactorial and heterogeneous disorder, it is now widely accepted that preeclampsia is stratified depending on the time of onset into: i) early-onset PE (EOPE) manifested before 34 weeks of gestation, and ii) late-onset PE (LOPE) manifested from 34 weeks of gestation. Although EOPE and LOPE share the same diagnostic criteria, these two phenotypes of preeclampsia lead to different outcomes. EOPE is commonly associated with FGR, abnormal uterine artery Doppler often leading to preterm birth and higher risk of post-pregnancy morbidities5,6. On the other hand, LOPE appears to be a less severe disorder, often with normal or slightly increased uterine resistance index and a low rate of FGR6,7. Distinct delineation between EOPE and LOPE is still not well understood, with most patients with preeclampsia presenting elements of both pathologies proposing a clinical spectrum for preeclampsia. The lack of untargeted discovery studies involving ‘omics’ analyses has impeded understanding of the molecular differences between these two phenotypes of preeclampsia. Notably, a study from 20058 utilised a proteomics approach using urine samples from a cohort of pregnant women with EOPE and healthy controls, however the differences between EOPE and LOPE were not elucidated. Another more recent bioinformatics study, identified overlapping pathogenic mechanisms between preeclampsia, hypertension and heart disease but could not stratify between EOPE and LOPE due to underreported of data related to individual phenotypes9. In this study, we conducted an unbiased, comprehensive proteomics investigation using plasma samples collected from patients with EOPE (n=17) and LOPE (n=11), compared with age- and BMI-matched normotensive controls (n=18). The use of plasma samples is able to better reflect the pathogenesis of EOPE and LOPE as systemic conditions centred by widespread endothelial dysfunction.
2023-03-11 | PXD026931 | Pride
Project description:The aim of the study was to compare gene expression profiles in decidua basalis from cases with complicated pregnancies to those from healthy pregnant controls. Cases included pregnant women with preeclampsia (PE) and/or fetal growth restriction (FGR). Decidual tissue was obtained by vacuum suction of the placental bed after the placenta was delivered. Women with PE and/or FGR were included as cases. PE was defined as persistent hypertension (blood pressure (BP) ¡Ý 140/90 mm Hg), plus proteinuria (¡Ý0.3g/24 h or ¡Ý2+ according to a dipstick test), developing after 20 weeks of pregnancy. FGR implied birth weight under 2 standard deviations (SD) below the expected birth weight, as related to gestational age (GA) and sex. Due to tissue sampling procedures, only cases delivered by cesarean section (CS) were included. Healthy women with normal pregnancies, undergoing CS for various reasons considered irrelevant to the aim of this study (e. g. breech presentation and previous CS), served as controls. Tissue was immediately submerged in a RNA stabilisation solution (RNAlater, Ambion, Huntingdon, U.K.), incubated at 4¡ãC overnight and stored at -80¡ãC
2007-08-31 | E-MEXP-1050 | biostudies-arrayexpress
Project description:Preeclampsia (PE) is a multi-system disorder that is primarily characterised by new-onset hypertension accompanied by proteinuria during gestation. This disease affects 3-5% of all pregnancies and is one of the leading causes of maternal and perinatal morbidity and mortality. In this work, placental samples were collected from PE and control patients. RNA-seq was performed to identify differences in gene expression. Significantly differentially expressed genes between the PE and control samples included 68 up-regulated and 52 down-regulated genes. This study may provide further insight in the mechanisms of PE and function as preventive, predictive and therapeutic measures.
2020-08-24 | GSE143953 | GEO
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Experiment Overall Design: 6 affymetrix human expression chips (GPL570) were analyzed. Experiment Overall Design: They represent 3 tissues (pooled from 10 individuals each) from patients with preeclampsia and from patients with uneventful pregnancy (collected by cesaraen section). Tissues from patients with uneventful pregnancy are the controls in comparison to tissues of patients with preeclampsia.
2008-06-14 | E-GEOD-6573 | biostudies-arrayexpress
Project description:We have demonstrated that the etiology of preeclampsia (PE) is associated with protein aggregation, a pathologic paradigm observed in neurodegenerative diseases, and that impaired autophagy contributes to accumulation of protein aggregates. In search of therapeutic options for preeclampsia that inhibit protein aggregation and restore autophagy, we screened several small molecules and identified a class of disaccharides that may prove to be highly efficacious to treat and prevent this severe pregnancy complication. We used the human serum-based humanized PE mouse model to assess the effect of disaccharides on the onset of the syndrome. Mice were i.p. injected with vehicle, disaccharides (2g/kg) at gd9, gd11, and gd14. At gd17, urine was collected, blood pressure was measured, fetal weight was recorded, and placenta was collected and subjected to immunostaining and RNA sequencing. Trehalose and Lactotrehalose inhibited hypoxia-induced accumulation of aggregates and restored impaired autophagy-lysosomal machinery. Disaccharide administration significantly restored normal pregnancy features in PE mice as characterized by normalization of hypertension, proteinuria, growth restriction, and kidney injury. RNA-seq analysis identified some novel genes and pathways that are related to preeclampsia and normalized by disaccharides.
2023-11-01 | GSE202129 | GEO
Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Keywords: disease comparison, disease state
2007-01-01 | GSE6573 | GEO