Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3317060.fastq.gz | Fastqsanger.gz | |||
| SRR3317070.fastq.gz | Fastqsanger.gz | |||
| SRR3317080.fastq.gz | Fastqsanger.gz | |||
| SRR3317090.fastq.gz | Fastqsanger.gz | |||
| SRR3317100.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Amnion as a surrogate tissue reporter of the effects of maternal preeclampsia on the fetus
| PRJNA316989 | ENA
Project description:Amnion as a surrogate tissue reporter of the effects of maternal preeclampsia on the fetus [RNA-Seq]
| PRJNA316992 | ENA
Project description:Background: Preeclampsia, traditionally characterized by high blood pressure and proteinuria, is a common pregnancy complication, which affects 2-8% of all pregnancies. Although children born to women with preeclampsia have a higher risk of hypertension in later life, the mechanism of this increased risk is unknown. DNA methylation is an epigenetic modification that has been studied as a mediator of cellular memory of adverse exposures in utero. Since each cell type in the body has a unique DNA profile, cell subtype composition is a major confounding factor in studies of tissues with heterogeneous cell types. The best way to avoid this confounding effect is by using purified cell types. However, the use purified cell types in large cohort translational studies is difficult. The amnion, the inner layer of the fetal membranes of placenta, is derived from the epiblast and consists of two cell types, which are easy to isolate from the delivered placenta. In this study, we demonstrate the value of using amnion samples for DNA methylation studies, revealing distinctive patterns between fetuses exposed to preeclampsia or hypertension and fetuses from normal pregnancies. Results: We performed a genome-wide DNA methylation analysis, HELP-tagging, on 62 amnion samples from placentas of uncomplicated, normal pregnancies, and those with complications of preeclampsia or hypertension. Using a regression model approach, we found 123, 85 and 99 loci with high confidence hypertension-associated, proteinuria-associated and hypertension and proteinuria-associated DNA methylation changes, respectively. We also found that these differentially methylated regions overlap loci previously reported as differentially methylated regions in preeclampsia. Conclusions: Our findings support prior observations that preeclampsia is associated with changes of DNA methylation near genes that have previously been found to be dysregulated in preeclampsia. We propose that amnionic membranes represent a valuable surrogate fetal tissue on which to perform epigenome-wide association studies of adverse intrauterine conditions.
2016-06-17 | GSE79782 | GEO
Project description:Background: Preeclampsia, traditionally characterized by high blood pressure and proteinuria, is a common pregnancy complication, which affects 2-8% of all pregnancies. Although children born to women with preeclampsia have a higher risk of hypertension in later life, the mechanism of this increased risk is unknown. DNA methylation is an epigenetic modification that has been studied as a mediator of cellular memory of adverse exposures in utero. Since each cell type in the body has a unique DNA profile, cell subtype composition is a major confounding factor in studies of tissues with heterogeneous cell types. The best way to avoid this confounding effect is by using purified cell types. However, the use purified cell types in large cohort translational studies is difficult. The amnion, the inner layer of the fetal membranes of placenta, is derived from the epiblast and consists of two cell types, which are easy to isolate from the delivered placenta. In this study, we demonstrate the value of using amnion samples for DNA methylation studies, revealing distinctive patterns between fetuses exposed to preeclampsia or hypertension and fetuses from normal pregnancies. Results: We performed a genome-wide DNA methylation analysis, HELP-tagging, on 62 amnion samples from placentas of uncomplicated, normal pregnancies, and those with complications of preeclampsia or hypertension. Using a regression model approach, we found 123, 85 and 99 loci with high confidence hypertension-associated, proteinuria-associated and hypertension and proteinuria-associated DNA methylation changes, respectively. We also found that these differentially methylated regions overlap loci previously reported as differentially methylated regions in preeclampsia. Conclusions: Our findings support prior observations that preeclampsia is associated with changes of DNA methylation near genes that have previously been found to be dysregulated in preeclampsia. We propose that amnionic membranes represent a valuable surrogate fetal tissue on which to perform epigenome-wide association studies of adverse intrauterine conditions.
2016-06-17 | GSE79781 | GEO
Project description:Normal pregnancy requires adaptations of the maternal vasculature. During preeclampsia these adjustments are not well established, resulting in maternal hypertension and proteinuria. The effects of preeclampsia on the maternal vasculature are not yet fully understood. We aimed to identify gene expression differences in the aorta between non pregnant, healthy pregnant, and experimental preeclamptic rats using a genome wide approach. Whole aortic tissue was isolated from rats with low-dose LPS-induced preeclampsia, healthy pregnant and non-pregnant rats. Gene expression was measured by a whole genome microarray.
2017-11-01 | GSE96610 | GEO
Project description:During pregnancy, immune responses must balance fetal protection from infections with tolerance of the semi-allogeneic fetus. However, the mechanisms regulating maternal-fetal tolerance remain poorly understood. Recently, we identified KIR+CD8+ T cells as a previously underappreciated regulatory subset important for suppressing self-reactivity in human autoimmune and infectious diseases. To better understand what other roles these cells might play, we asked whether they are active during pregnancy. We first observed an increased frequency of KIR+CD8+ T cells in the peripheral blood of pregnant women at the second trimester, especially in those carrying a male fetus. In vitro, KIR+CD8+ T cells inhibited the alloreactive responses of maternal T cells against irradiated cord blood cells and suppressed HY-specific CD8+ T cells from mothers with a male fetus. Therefore, the higher induction of KIR+CD8+ T cells in mothers carrying a male fetus may help suppress additional allogenic responses triggered by Y chromosome antigens. Longitudinal analysis showed that KIR+CD8+ T cells undergo expansion and differentiate into functional cytotoxic cells during pregnancy. Single cell RNA-seq analysis of decidual CD8+ T cells from early pregnancy revealed elevated number and activity of KIR+ CD8+ T cells at the maternal-fetal interface. In addition, increased levels of KIR+CD8+ T cells correlated with pregnancy disorders (e.g., spontaneous abortion and preeclampsia). Taken together, our findings suggest an important role of KIR+CD8+ T cells in the maintenance of maternal tolerance by suppressing fetal-specific alloreactive T cells. They may also be useful as predictive biomarkers or drug targets for human pregnancy disorders.
2025-08-01 | GSE281341 | GEO
Project description:Epidemiological studies suggest that maternal exposures to environmental chemicals may be linked to spontaneous preterm birth. Mechanistic studies are needed to provide support to these hypotheses; however, existing in vitro models do not replicate the human feto-maternal barriers beyond placenta. The recently developed four-cell (human immortalized maternal decidua, chorion trophoblast, amnion mesenchymal, and amnion epithelial cells) Feto-Maternal interface Organ-On-Chip (FMi-OOC) enables studies of chemical effects on the decidua, chorion and amnion, maternal and fetal tissues that are critically important for maintaining full-term pregnancy. We tested four environmental compounds that have been associated with preterm birth – dichlorodiphenyltrichloroethane (DDT-o,p’), bisphenol A (BPA), 2,2'4,4'-tetrabromodiphenyl ether (PBDE-47), and perfluorooctanoic acid (PFOA). First, concentration-response effects of these chemicals were tested on maternal decidua cells in 96-well plates. Then, experiments were performed in FMi-OOC containing four fetal-maternal cell types arranged into four concentric chambers, mimicking the in utero cell topology. Compounds were added to the maternal (i.e., decidua) chambers, and chemical propagation, cell viability and proinflammatory cytokines (IL-6, IL-8, GM-CSF, TNF-α) were measured in decidua, chorion trophoblast, amnion mesenchymal, and amnion epithelial cells for up to 72 hrs. Minimal propagation of test compounds to fetal chambers was observed and tested concentrations were non-cytotoxic. Treatment-associated increase in cytokine production was observed for all compounds, with PFOA and BPA showing the strongest effects and amnion epithelial cells being the most responsive. We demonstrate how the multi-cellular FMi-OOC model can be used to study paracrine signaling in complex human tissues such as fetal-maternal interface. In addition, these studies provide mechanistic support for the plausibility of the epidemiological associations between maternal exposures to tested compounds and preterm birth. We show that upon maternal exposure, albeit at concentrations exceeding reported human blood levels by 1 to 2 orders of magnitude, fetal membranes attain a pro-inflammatory state, a potential trigger for preterm birth.
2025-07-28 | GSE295995 | GEO
Project description:The placenta plays a crucial role in the normal growth and development in mammals by serving as an interface for nutrients, respiratory gases and physiological signals between the mother and fetus. Here we use a novel embryo transfer system in mice to identify the major physiological pathways in the placenta that are principally influenced by altered maternal environment. Embryos of identical genotype were transferred at the one cell stage into surrogate mothers either of the same strain or from a different strain. We analyzed the relative effects of maternal and fetal genotype on fetal weight, placental weight and the placental transcriptome at E18.5. The results show that maternal genotype overrides fetal genotype as the principal regulator of fetal weight (p<0.0001). Microarray analysis of the transcriptome in placentas revealed that a small fraction (0.25%) of placental genes are specifically regulated by maternal genotype (p<0.05, FDR<0.10). Pathway analysis of these genes using the programs Gene Ontology and MetaCore from GeneGO inc. revealed highest statistical significance in signaling pathways that regulate cell growth and lipid metabolism. These results provide a mechanistic understanding of important molecular pathways involved in maternal regulation of fetal growth and development.
2010-08-06 | E-MEXP-2479 | biostudies-arrayexpress
Project description:The human placenta (the extra-embryonic organ in which the fetus is made) is essential for conception and protection of the fetus during pregnancy. Extravillous trophoblasts (EVT) from placental villi infiltrate the decidua and convert maternal arteries into high-conductance vessels. Defects in trophoblast invasion and arterial conversion in early pregnancy are at the root of common pregnancy disorders such as preeclampsia. Here, we generated ecdysone and chorionic monocytic profiles across different gestational weeks spanning the 22-45 year age range, which allowed us to resolve the differentiation trajectory of trophoblast cells at implantation and its relationship with maternal age. We used this age atlas to identify age nodes of placental implantation change, revealing patterns of EVT implantation in advanced versus normal maternal age. Our data provide a comprehensive analysis of post-bedding trophoblast cell differentiation and may inform the design of experimental models of the placenta in early human pregnancy.
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Project description:Maternal stressors as psychophysical stress and obesity might share converging inflammatory/OS related pathways, disrupting fetal brain development, assuming a key role for the placenta in conveying maternal stressful mediators to the fetus. To test such hypothesis, we used two different mouse models mimicking, respectively, maternal psychophysical stress and maternal obesity and anlyased by LFQ-DIA mass spectrometry the placental tissue.
2023-07-10 | MSV000092388 | MassIVE