Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73377 | GEO | 2015/09/24

SECONDARY ACCESSION(S): PRJNA296821

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway.

Project description:Preeclampsia is a potentially fatal pregnancy disorder affecting millions of women around the globe. Dysregulation in gene and protein expression within key biological pathways controlling angiogenesis has been implicated in the development of preeclampsia. Altered CpG methylation, a type of epimutation, may underlie this pathway dysregulation. In the present study, placental tissue from preeclamptic cases and normotensive controls was analyzed for genome-wide differential CpG methylation and concomitant changes in gene expression. A set of 123 genes, representing 19.9% of all genes with altered CpG methylation, was associated with functional changes in transcript levels. Underscoring the complex relationships between CpG methylation and gene expression, here hypermethylation was never associated with gene silencing, nor was hypomethylation always associated with gene activation. Moreover, the genomic region of the CpG mark was important in predicting the relationship between CpG methylation and gene expression. The 123 genes were enriched for their involvement in the transforming growth factor beta (TGF-β) signaling pathway, a known regulator of placental trophoblast invasion and migration. This is the first study to identify CpG hypomethylation as an activator of TGF-β-associated gene expression in the preeclamptic placenta. The results suggest functional epimutations are associated with preeclampsia disease status and the identified genes may represent novel biomarkers of disease.

| S-EPMC4624949 | biostudies-literature

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-24 | E-GEOD-73377 | biostudies-arrayexpress

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [methylation]

Project description:Placental Tissue Samples from 36 women (17 normotensive women, denoted with a P, and 19 preeclamptic women, denoted with a Q) were analyzed for differenital methylation Preeclamptic womene were compared direclty to normotensive women controlling for gestational age, race, maternal age, and baby sex 36 samples were analyzed, 18 in each group

2015-09-24 | E-GEOD-73375 | biostudies-arrayexpress

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [methylation]

2015-09-24 | GSE73375 | GEO

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [gene expression]

2015-09-24 | E-GEOD-73374 | biostudies-arrayexpress

Epigenetics and Preeclampsia: Defining Functional Epimutations in the Preeclamptic Placenta Related to the TGF-β Pathway [gene expression]

2015-09-24 | GSE73374 | GEO

miRNAs as common regulators of the transforming growth factor (TGF)-? pathway in the preeclamptic placenta and cadmium-treated trophoblasts: Links between the environment, the epigenome and preeclampsia.

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/placenta. While the etiology is unknown, poor placentation due to aberrant signaling of growth and angiogenic factors has been postulated as a causal factor 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-?) pathway. Genes within the TGF-? pathway displayed increased expression in both the preeclamptic placenta and Cd-treated trophoblasts. In addition, miRNAs that target the TGF-? 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-? pathway. Results from this study provide future targets for PE treatment.

| S-EPMC5156314 | biostudies-literature

miRNAs as Common Regulators of the Transforming Growth Factor (TGF)-β Pathway in the Preeclamptic Placenta and Cadmium-treated Trophoblasts: Links between the Environment, the Epigenome and Preeclampsia

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

Landscape of transcriptional deregulations in the preeclamptic placenta.

Project description:Preeclampsia is a pregnancy disease affecting 5 to 8% of pregnant women and a leading cause of both maternal and fetal mortality and morbidity. Because of a default in the process of implantation, the placenta of preeclamptic women undergoes insufficient vascularization. This results in placental ischemia, inflammation and subsequent release of placental debris and vasoactive factors in the maternal circulation causing a systemic endothelial activation. Several microarray studies have analyzed the transcriptome of the preeclamptic placentas to identify genes which could be involved in placental dysfunction. In this study, we compared the data from publicly available microarray analyses to obtain a consensus list of modified genes. This allowed to identify consistently modified genes in the preeclamptic placenta. Of these, 67 were up-regulated and 31 down-regulated. Assuming that changes in the transcription level of co-expressed genes may result from the coordinated action of a limited number of transcription factors, we looked for over-represented putative transcription factor binding sites in the promoters of these genes. Indeed, we found that the promoters of up-regulated genes are enriched in putative binding sites for NFkB, CREB, ANRT, REEB1, SP1, and AP-2. In the promoters of down-regulated genes, the most prevalent putative binding sites are those of MZF-1, NFYA, E2F1 and MEF2A. These transcriptions factors are known to regulate specific biological pathways such as cell responses to inflammation, hypoxia, DNA damage and proliferation. We discuss here the molecular mechanisms of action of these transcription factors and how they can be related to the placental dysfunction in the context of preeclampsia.

| S-EPMC3681798 | biostudies-literature

Evaluation of circulating placenta-related long noncoding RNAs as potential biomarkers for preeclampsia.

Project description:Increasing evidence has indicated that circulating placental RNAs may reflect the pathophysiology of the placenta. In the current study, circulating placenta-related long noncoding RNAs (lncRNAs) were evaluated as potential biomarkers for preeclampsia (PE). Two parts of the case-control study were simultaneously executed, including the following sets: 52 patients with late-onset PE (LOPE) (diagnosed after 34 weeks) and 52 gestational age (GA)-matched controls; 58 patients with early-onset PE (EOPE) (diagnosed before 34 weeks) and 58 GA-matched controls. LncRNA expression was detected in the placenta analysis part, and the participants were delivered by caesarean sections. The levels of circulating placenta-associated lncRNAs were measured in the plasma analysis part and all pregnant women were included. Using microarray analysis, 163 differentially expressed lncRNAs were identified in placental samples from patients with LOPE, some of which were also detected in plasma samples from pregnant women. There were significant positive correlations between plasma, and placental expression levels of NONHSAT116812 and NONHSAT145880, which in plasma provided high diagnostic efficiencies for LOPE and EOPE. The present study demonstrated that circulating placenta-associated lncRNAs, paticularly NONHSAT116812 and NONHSAT145880 have potential as biomarkers for PE.

| S-EPMC5920431 | biostudies-literature