Single cell RNA sequencing of placenta in patients with early onset preeclampsia
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE282038 | GEO | 2025/04/16
REPOSITORIES: GEO
Similar Datasets
Project description:Introduction: To determine the miRNA expression profile in placentas complicated by Preeclampsia (PE) and compare it to uncomplicated pregnancies. Methods: Sixteen placentas from women with PE, including 11 with early onset PE (EOPE) and 5 with late onset PE (LOPE), as well as 8 from uncomplicated pregnancies were analyzed using miRNA microarrays. For statistical analyses the MATLAB® simulation environment was applied. The over-expression of miR-518a-5p was verified using Quantitative Real-Time Polymerase Chain Reaction. Results: Overall, 44 miRNAs were found deregulateddysregulated in PE complicated placentas. Statistical analysis revealed that miR-431, miR-518a-5p and miR-124* were over-expressed in EOPE complicated placentas as compared to controls whereas miR-544 and miR-3942 were down-regulated in EOPE. When comparing the miRNA expression profile in cases with PE and PE- growth restricted fetuses (FGR), miR-431 and miR-518a-5p were found over-expressed in pregnancies complicated by FGR. Additionally, up- regulation of miR-124, miR-423-3p and miR-518a-5p was associated with proteinuria. Discussion: Specific miRNAs can differentiate EOPE and LOPE from uncomplicated pregnancies representing putative PE-specific diagnostic biomarkers. Among them, miR-518a-5p emerged as a potential diagnostic indicator for EOPE cases as well as for FGR and proteinuria associated PE complicated placentas designating its potential link to the severity of the disease.
2017-09-07 | GSE103542 | GEO
Project description:Introduction. Preeclampsia (PE) carries increased risks of cardiovascular- and metabolic diseases in mothers and offspring during the life course. While the severe early-onset PE (EOPE) phenotype originates from impaired placentation in early pregnancy, late-onset PE (LOPE) is in particular associated with pre-existing maternal cardiovascular- and metabolic risk factors. We hypothesize that PE is associated with altered epigenetic programming of placental and fetal tissues and that these epigenetic changes might elucidate the increased cardiovascular- and metabolic disease susceptibility in PE offspring. Methods. A nested case-control study was conducted in The Rotterdam Periconceptional Cohort comprising 13 EOPE, 16 LOPE, and three control groups of 36 uncomplicated pregnancies, 27 normotensive fetal growth restricted (FGR) and 20 normotensive preterm birth (PTB) complicated pregnancies. Placental tissue, newborn umbilical cord blood leucocytes (UC-WBC) and umbilical vein endothelial cells (HUVEC) were collected and DNA methylation of cytosine-guanine dinucleotides was measured by the Illumina HumanMethylation450K BeadChip. An epigenome-wide analysis was performed by using multiple linear regression models. Results. Epigenome-wide tissue-specific analysis between EOPE and PTB controls revealed 5001 mostly hypermethylated differentially methylated positions (DMPs) in UC-WBC and 869 mostly hypomethylated DMPs in placental tissue, situated in or close to genes associated with cardiovascular-metabolic developmental pathways. Discussion. This study shows differential methylation in UC-WBC and placental tissue in EOPE as compared to PTB, identifying DMPs that are associated with cardiovascular system pathways. Future studies should examine these loci and pathways in more detail to elucidate the associations between prenatal PE exposure and the cardiovascular disease risk in offspring.
2017-09-06 | GSE103253 | GEO
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:For understanding the relationship of preeclampsia and placental methylation,we performed an epigenome-wide association study in a Chinese cohort containing 22 early-onset preeclampsia patients and 20 normal controls. We used Illumina Infinium HumanMethylation450k BeadChip for detecting the methylation level, and used placental genomic DNA as sample. most of the significant CpG sites were hypomethylated in EOPE in the Chinese cohort.
2019-06-30 | GSE125605 | GEO
Project description:Placental disorders contribute to pregnancy complications including preeclampsia (PE) and fetal growth restriction (FGR), but debate regarding their specific pathobiology persists. Our objective was to apply transcriptomics with weighted gene correlation network analysis (WGCNA) to further clarify the placental dysfunction in these conditions.
2023-08-25 | GSE203507 | GEO
Project description:Early onset preeclampsia (EOPE) affects about 0.4% of pregnancies and is characterized by impaired trophoblast (TB) invasion, resulting in a poorly perfused placenta. Here we have used an in vitro model for mimicking early trophoblast development to determine how early placental development differs between normal pregnancies and those affected by EOPE. Induced pluripotent stem cells (iPSC) were generated from umbilical cords of infants born to mothers who had EOPE and from controls. These iPSC were converted to TB, by exposing them to BMP4 and inhibitors of ACTIVIN A and FGF2 signaling (BAP treatment), under 5 % and 20 % O2, hypothesizing that 20% O2 would act as a stressor. Two embryonic stem cell lines (ESC; H1 and H9), 8 control (CTL) iPSC and 14 EOPE iPSC were tested to assess how well the differentiated TB cells invaded through a Matrigel-coated membrane.
2018-12-31 | GSE119265 | GEO
Project description:Fetal growth restriction (FGR) is a heterogeneous disorder of pregnancy associated with pathologically low fetal and neonatal weights. We hypothesized that FGR consists of multiple placental subtypes, similar to what we have observed in preeclampsia. To address this hypothesis, we assembled a fetal growth-focused human placental microarray data set (N=97) consisting of 20 new normotensive suspected FGR samples (below), in addition to term controls (N=26) and hypertensive suspected FGR samples (N=51) from GSE75010.
2018-10-13 | GSE100415 | GEO
Project description:Preeclampsia, a significant cause of maternal and perinatal morbidity and mortality, remains poorly understood in terms of its pathogenesis. This study aims to uncover novel and effective biomarkers for preeclampsia by conducting a comparative analysis of differential proteins in placentas from early-onset preeclampsia (EOPE) and normal pregnancies. Utilizing tandem mass tag (TMT)-based quantitative proteomics, we identified differentially expressed proteins in placental tissues from 15 EOPE patients and 15 normal pregnant women. These proteins were subsequently validated using parallel reaction monitoring (PRM). Our analysis revealed a total of 59 differentially expressed proteins, with 25 up-regulated and 34 down-regulated in EOPE placental tissues compared to those from normal pregnancies. Validation through PRM confirmed the differential expression of 6 proteins. Our findings suggest these 6 proteins could play crucial roles in the pathogenesis of EOPE, highlighting the potential involvement of the Estrogen signaling pathway and Dilated cardiomyopathy (DCM) pathway in the development of preeclampsia.
2024-08-20 | PXD055025 |
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 is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.
2021-12-13 | GSE190639 | GEO