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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [methylation]

ABSTRACT: Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. Specific transcriptional and epigenetic perturbations associated with GDM status included alterations in the major histocompatibility complex (MHC) region, which were validated in an independent cohort, the Rhode Island Child Health Study. Gene ontology enrichment among gene regulation influenced by GDM revealed an over-representation of immune response pathways among differential expression, reflecting these coordinated changes in the MHC region. Our study represents the largest investigation of transcriptomic and methylomic differences associated with GDM, providing comprehensive insight into the molecular basis of GDM induced fetal (re)programming. Bisulphite converted DNA extracted from the placentas (maternal-side) of 41 clinically-confirmed cases of GDM and 41 pregnancies without maternal complications were hybridised to the Illumina Infinium HumanMethylation450 Beadchips

ORGANISM(S): Homo sapiens

SUBMITTER: Alexandra Binder

PROVIDER: E-GEOD-70453 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [gene expression]

Project description:Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. Specific transcriptional and epigenetic perturbations associated with GDM status included alterations in the major histocompatibility complex (MHC) region, which were validated in an independent cohort, the Rhode Island Child Health Study. Gene ontology enrichment among gene regulation influenced by GDM revealed an over-representation of immune response pathways among differential expression, reflecting these coordinated changes in the MHC region. Our study represents the largest investigation of transcriptomic and methylomic differences associated with GDM, providing comprehensive insight into the molecular basis of GDM induced fetal (re)programming. RNA extracted from the placentas (maternal-side) of 30 clinically-confirmed cases of GDM and 25 pregnancies without maternal complications was hybridised to the GeneChip® Human Transcriptome Array 2.0 (Affymetrix). Four samples were run in triplicate.

2015-08-03 | E-GEOD-70493 | biostudies-arrayexpress

Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [gene expression]

2015-08-03 | GSE70493 | GEO

Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [methylation]

2015-08-03 | GSE70453 | GEO

Serum exosomal miRNA profile in pregnancies with gestational diabetes based on pancreatic β-cell function

Project description:Pancreatic β-cell function impairment is a key mechanism for developing gestational diabetes mellitus (GDM). Maternal and placental exosomes regulate maternal and placental responses during hyperglycemia. Studies have associated exosomal micro RNAs (miRNAs) with GDM development. To date, no studies have been reported that evaluate the profile of miRNAs present in maternal and placental exosomes in the early stages of gestation from pregnancies that develop GDM. We used microarrays to assess whether early pregnancy maternal and placental exosomal miRNA profiles vary according to pancreatic β-cell function in women who will develop GDM (preGDM).

2024-02-29 | GSE243374 | GEO

Epigenetic signatures of gestational diabetes mellitus on ATP5A1, PRKCH, SLC17A4 and HIF3A cord blood methylation

Project description:Background: Intrauterine exposure to gestational diabetes mellitus (GDM) confers a lifelong increased risk for metabolic and other complex disorders to the offspring. GDM-induced epigenetic modifications modulating gene regulation and persisting into later life are generally assumed to mediate these increased disease risks. To identify candidate genes for fetal programming, we compared genome-wide methylation patterns of fetal cord bloods (FCBs) from GDM and control pregnancies. Methods and Results: Using Illumina's 450K methylation arrays and following correction for multiple testing, 65 CpG sites (52 of which are associated with genes) displayed significant methylation differences between GDM and control samples. Three of four candidate genes, ATP5A1, PRKCH, and SLC17A4, from our methylation screen and one, HIF3A, from the literature were validated by bisulfite pyrosequencing. The GDM effect on FCB methylation was more pronounced in women with insulin-dependent GDM who had a more severe metabolic phenotype than women with dietetically treated GDM. However, the effect remained significant after adjustment for the maternal BMI and gestational week in a multivariate regression model. Conclusions: Our study supports an association between maternal GDM and the epigenetic status of the exposed offspring. Consistent with a multifactorial disease model, the observed FCB methylation changes are of small effect size but affect multiple genes/loci. The identified genes are primary candidates for transmitting GDM effects to the next generation. They also may provide useful biomarkers for the diagnosis and prognosis of adverse prenatal exposures and assessing the success of interventions during pregnancy.

2017-03-29 | GSE88929 | GEO

Effect of O-GlcNAc Transferase (OGT) siRNA in trophoblastic BeWo cells

Project description:Every year, about 18 million babies are born from mothers with gestational diabetes mellitus (GDM). While diabetic symptoms usually resolve after delivery, lasting complications can occur for both mother and child, including fetal overgrowth, type 2 diabetes (T2D), cardiovascular diseases, and obesity. The rapid progression of GDM is unique to pregnancies, and likely arises from placental dysfunction. Indeed, stress, nutrition and fetal gender are thought to trigger changes in placental endocrine function, including metabolic hormones and inflammatory cytokines, potentially causing GDM. Nutrient-sensing O-GlcNAcylation and its enzyme O-GlcNAc Transferase (OGT, X-linked) has been previously identified as a placental biomarker of maternal stress particularly deleterious for male offspring. Thus, we wondered whether O-GlcNAcylation participate in GDM development in a sex-dependent manner. After demonstrating that OGT is largely downregulated in male GDM compared to healthy placentas, we knocked down OGT in male trophoblastic cells. We observed changes in placental hormones, cytokines and nutrient-sensing pathways, correlating with previously demonstrated disruption in GDM placentas. Altogether, this study demonstrates that OGT and O-GlcNAcylation are partly responsible for changes observed in GDM placenta and might be the cause of sexual dimorphism observed in this pathology.

2022-04-21 | GSE200983 | GEO

Integrating multi-omics analyses unveil protein features of gestational diabetes mellitus and preeclampsia

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2024-01-25 | PXD032981 | Pride

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function

Project description:We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. Further functional analysis demonstrated that GDM exposed cells have altered actin organization and barrier function. Our data indicate that exposure to GDM programs atypical morphology and barrier function in feto-placental endothelial cells by DNA methylation and gene expression change. The effects differ between AEC and VEC, indicating a stringent cell-specific sensitivity to adverse exposures associated with developmental programming in utero.

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Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function Changes

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