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PROVIDER: PRJNA296821 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [methylation]
| PRJNA296823 | ENA
Project description:Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [gene expression]
| PRJNA296822 | ENA
Project description:Preeclampsia (PE) is a pregnancy disorder characterized by high blood pressure and proteinuria that can cause adverse health effects in both mother and fetus. There is no current cure for PE other than delivery of the fetus. While the etiology is unknown, poor placentation of the placenta due to aberrant signaling of growth and angiogenic factors has been postulated as causal factors of PE. In addition, environmental contaminants, such as the metal cadmium (Cd), have been linked to placental toxicity and increased risk of developing PE. Here, we use a translational study design to investigate genomic and epigenomic alterations in both placentas and placental trophoblasts, focused on the angiogenesis-associated transforming growth factor-beta (TGF-β) pathway. Genes within the TGF-β pathway displayed increased expression in both the preeclamptic placenta and Cd-treated trophoblasts. In addition, miRNAs that target the TGF-β pathway were also significantly altered within the preeclamptic placenta and Cd-treated trophoblasts. Integrative analysis resulted in the identification of a subset of Cd-responsive miRNAs, including miR-26a and miR-155, common to preeclamptic placentas and Cd-treated trophoblasts. These miRNAs have previously been linked to PE and are predicted to regulate members of the TGF-β pathway. Results from this study provide future targets for PE treatment.
2016-07-12 | GSE84260 | GEO
Project description:Preeclampsia is a disease of pregnant women, which is characterized by hypertension, proteinuria and chronic inflammation. There is a growing body of evidence that cause of preeclampsia lies within immunological aspect of pregnancy. This study aimed to analyze the role of CD74 in preeclampsia with a focus on its influence on communication between placental macrophages (Hofbauer cells) and trophoblasts. We have found CD74 to be highly dysregulated in preeclamptic placenta by real-time RT-PCR and Western blot methods. We identified Hofbauer cells to express the highest levels of CD74 in placenta by immunofluorescence and flow cytometry and that CD74 in preeclamptic Hofbauer cells is lower than in controls. We have performed a transcriptome analysis on human blood monocyte-derived macrophages that were non- or IL-4-activated and treated with small interfering RNA against CD74 (siRNA CD74) or non-targeting siRNA (siRNA non-targeting) as control.
2015-04-29 | E-MTAB-3309 | biostudies-arrayexpress
Project description:Prenatal development is a critical period for programming of neurological disease. Preeclampsia, a pregnancy complication involving oxidative stress in the placenta, has been associated with long-term health implications for the child, including an increased risk of developing schizophrenia and autism spectrum disorders in later life. We have shown previously, in a rodent model of placental oxidative stress, that culture medium conditioned by the placenta alters neuronal characteristics when applied to primary cortical cultures in vitro and mimics many of the neurodevelopmental changes observed in the offspring brain. To further investigate if molecules released by the placenta may be important mediators in foetal programming of the brain, we analysed if placental tissue delivered from patients with preeclampsia secreted molecules that could affect cortical cells in culture. Application of culture medium conditioned by preeclamptic placentae to mixed cortical cultures caused changes in neurons and astrocytes that were related to key changes observed in brains of patients with schizophrenia and autism, including effects on dendrite lengths, astrocyte number as well as glutamate and GABA receptors. Treatment of the placental explants with an antioxidant prevented neuronal abnormalities. Furthermore, we identified that bidirectional communication between neurons and astrocytes, potentially via glutamate, is required to produce the effects of preeclamptic placenta medium on cortical cells. Analysis of possible signalling molecules in the placenta conditioned medium showed that the secretion profile of extracellular microRNA, small posttranscriptional regulators, was altered in preeclampsia and partially rescued by antioxidant treatment of the placental explants. Predicted targets of these differentially abundant microRNAs were linked to neurodevelopment and the placenta. The presented study provides further evidence that the diseased placenta may release factors that damage cortical cells in the brain and suggests the possibility of targeted antioxidant treatment of the placenta to prevent neurodevelopmental disorders.
2019-02-11 | GSE110786 | GEO
Project description:Preeclampsia is a devastating hypertensive disorder of pregnancy that afflicts between 5-10% of pregnancies in the US, with a higher prevalence in the southern regions of the United States. Black pregnant women are disproportionally at higher risk for preeclampsia onset and severity of disease than other racial groups, including White women. Although this has been recognized in the maternal fetal medicine literature for many years, the underlying mechanism(s) for this racial disparity are unclear. One confounding issue with many studies of racial discrepancies in pregnant women is differences in comorbidities between racial groups. In our current study we were able to obtain a cohort of patients of self-identifying Black or White race that were overall matched for BMI, blood pressure, gestational age and parity and we hypothesized that genetic and placental markers of preeclampsia would be highest in our preeclampsia Black patients compared to healthy patients or White preeclampsia patients. We collected placenta tissue from this cohort of deliveries in Augusta, GA from both healthy and preeclamptic Black and White women (n=13-15). We measured expressions of several preeclampsia-implicated genes, as well as performed a placental morphological analysis and RNA sequencing of a subset of samples. Contrary to our hypothesis, our results from ddPCR analysis of genes associated with preeclampsia risk demonstrated that leptin, preproendothelin-1 (PPET-1) endothelial converting enzyme-1 (ECE-1) and soluble FMS-like tyrosine kinase-1 (sFlt-1) were higher in White preeclamptic women than in Black preeclamptic women. Our RNA sequencing analysis revealed that 136 genes significantly differed between White and Black normal pregnant patients, 288 genes differed between Black healthy and Black preeclampsia patients, while a striking 2394 genes significantly differed between White healthy and White preeclampsia patients and 2346 genes differed between White and Black preeclampsia patients. Placental histology analysis revealed that Black preeclampsia patients demonstrated a lower scoring of morphological pathologies associated with preeclampsia compared to White preeclampsia patients. Collectively, these data indicate that genetic predisposition to preeclampsia in White patients in the placenta differs greatly to that of Black patients, and that placental changes may be more subtle in Black patients that are at high risk for preeclampsia.
2026-07-06 | GSE303840 | GEO
Project description:The series is composed of thirty hybridizations for analysis of differentially expressed genes in normal placenta tissues from patients with normal labor and placenta tissues from patients with severe preeclampsia. Patients tissues samples were obtained from (Vasilis. Total RNA extraction was performed by using the MagNa Pure Compact RNA Isolation Kit (Roche Applied Science). Keywords: Gene expression study, Disease state Twenty-six out of 50 normal placentas were randomly selected to match with 17 preeclamptic placentas, accounting for parity. Microarrays were performed applying a direct comparison design.
2010-05-26 | E-GEOD-10588 | biostudies-arrayexpress
Project description:Fibrosis are known as one of the characteristic pathological findings of placenta in preeclampsia (PE). The mechanism underlying tissue injury when placental stroma is exposed to hypoxia and inflammatory stimulation is unclear. We focused on the relationship between pathogenesis of PE and placental fibrosis, and investigated the changes of fibrosis related factors (FRFs) in placental stroma. The mRNA levels of fibrosis related factors in PE were higher than those in normal pregnancy (NP). Those under hypoxia and by TGF-β stimulation were more prominent in PE compared with NP. The contraction rate of PE had significantly higher than that of NP. The significant elevation of plasma level of TGF-β in PE was indicated compared with those in NP.
2017-05-18 | GSE99007 | GEO
Project description:The placenta plays an important role as a regulator of fetal nutrition and growth throughout development and placental factors contribute to gestational abnormalities such as preeclampsia. This study describes the genome-wide gene expression profiles of a large (n=94) set of human placentas in order to uncover gene expression patterns (or molecular signatures) associated with preeclampsia and IUGR. Besides modulated modularity clustering and pathway analysis, a set of candidate miRNAs were predicted by Gene Set Enrichment Analysis (GSEA) based on differentially expressed genes. A case-control study was conducted to examine the expression patterns of these candidate miRNAs in human placentas 35 IUGR (including 8 technical repeats for batch effect), 19 preeclamptic and 40 control placentas included in this study were collected during the years of 2004-2008 and hybridized in two batches to microarrays. Samples were randomized across arrays to control for array and batch variability.
2012-02-07 | E-GEOD-35574 | biostudies-arrayexpress
Project description:The placenta plays an important role as a regulator of fetal nutrition and growth throughout development and placental factors contribute to gestational abnormalities such as preeclampsia. This study describes the genome-wide gene expression profiles of a large (n=60) set of human placentas in order to uncover gene expression patterns associated with preeclampsia. In addition to confirming changes in expression of soluble factors associated with preeclampsia such as sFLT1 (soluble fms-like tyrosine kinase-1), sENG (soluble endoglin), and INHA (inhibin alpha), we also find changes in immune-associated signaling pathways, offering a potential upstream explanation for the shallow trophoblast invasion and inadequate uterine remodeling typically observed in pathogenesis of preeclampsia. Notably, we also find evidence of preeclampsia-associated placental upregulation of sialic acid acetylesterase (SIAE), a gene functionally associated with autoimmune diseases. 23 preeclamptic, and 37 control placentas included in this study were collected during the years of 2004-2008 and hybridized in two batches to microarrays. Samples were randomized across arrays to control for array and batch variability.
2010-12-10 | E-GEOD-25906 | biostudies-arrayexpress