Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gestational Diabetes Induces Placental Genes for Chronic Stress and Inflammatory Pathways

ABSTRACT: A physiological state of insulin resistance is required to preferentially direct maternal nutrients toward the feto-placental unit, allowing adequate growth of the fetus. When women develop gestational diabetes mellitus (GDM), insulin resistance is more severe and disrupts the intrauterine milieu, resulting in accelerated fetal development with increased risk of macrosomia. As a natural interface between mother and fetus, the placenta is the obligatory target of such environmental changes. However, the molecular basis for the imbalance that leads to fetal, neonatal, and adult metabolic compromises is not well understood. We report that GDM elicits major changes in the expression profile of placental genes with a prominent increase in markers and mediators of inflammation. Within the 435 transcripts reproducibly modified, genes for stress-activated and inflammatory responses represented the largest functional cluster (18.5% of regulated genes). Upregulation of interleukins, leptin, and tumor necrosis factor-{alpha} receptors and their downstream molecular adaptors indicated an activation of pathways recruiting stress-activated protein/c-Jun NH2-terminal kinases. Transcriptional activation of extracellular matrix components and angiogenic activators pointed to a major structural reorganization of the placenta. Thus, placental transcriptome emerges as a primary target of the altered environment of diabetic pregnancy. The genes identified provide the basis to elucidate links between inflammatory pathways and GDM-associated insulin resistance. Keywords: other

ORGANISM(S): Homo sapiens

PROVIDER: GSE2956 | GEO | 2005/07/18

SECONDARY ACCESSION(S): PRJNA91963

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Exosomal RNA expression profiles and their prediction performance in gestational diabetes mellitus patients with macrosomia

Project description:Exosomal RNAs in cord blood may allow intercellular communication between maternal and fetus. We aimed to establish exosomal RNA expression profiles in cord blood exosomes from gestational diabetes mellitus (GDM) patients with macrosomia.We used microarray technology to establish the differential mRNA, lncRNA and circRNA expression profiles in cord blood exosomes from GDM patients with macrosomia compared with normal controls. A total of 98 mRNAs, 372 lncRNAs and 452 circRNAs were differentially expressed in cord blood exosomes from GDM patients with macrosomia. Pathway analysis showed the differential genes were associated with PI3K-Akt signaling pathway, JAK-STAT signaling pathway, TGF-beta signaling pathway, insulin resistance, glycerolipid metabolism, fatty acid degradation and mTOR signaling pathway. These results showed that exosomal RNAs are aberrantly expressed in the cord blood of GDM patients with macrosomia.

2022-01-21 | GSE194119 | GEO

Effects of intrauterine hyperglycemia on offspring development in gestational diabetes mellitus based on placental transcriptomics

Project description:Gestational diabetes (GDM) refers to diabetes diagnosed as diabetes in the second or third trimester of pregnancy, but not obvious before pregnancy. It is one of the most common complications of pregnancy, which can lead to perinatal asphyxia, neonatal hypoglycemia, macrosomia, cardiovascular abnormalities, obesity and other short-term and long-term adverse outcomes of the offspring. This study explores the differential expression of transcriptome between GDM and non GDM placenta, and explores the impact of subtle metabolic changes in the placenta on fetal growth and development during GDM in pregnant women.

2024-07-30 | GSE263483 | GEO

Human Cytomegalovirus modifies placental small extracellular vesicle secretion and composition to enhance infection of fetal recipient cells

Project description:Human cytomegalovirus (hCMV) primo-infection, reinfection and/or reactivation is a major issue during pregnancy and affects 1% of live births in western countries, making hCMV the most frequently transmitted virus in utero. Despite the extensive research conducted so far, the pathophysiology of this congenital infection remains unclear. Recently, increasing evidence point out the role of small extracellular vesicles (sEVs) in cell-cell communication underlying the feto-placenta-maternal dialogue during pregnancy. In this study, we examined the impact of hCMV infection on the protein composition and function of placental sEVs. We observed that infection of placental cells led to an alteration of protein composition of their secreted sEVs, suggesting that placental sEVs may acquire a proviral phenotype. Functional studies performed on fetal recipient cells, notably neural stem cells, confirmed the ability of sEVs produced by infected cells to facilitate further infection of naive recipient cells. Altogether, our study demonstrates that placental sEVs are key players of hCMV pathophysiology during congenital infection, and may favor the transmission of the virus towards the fetus.

2022-10-13 | PXD029146 | Pride

Gestational diabetes mellitus alters placental structure, efficiency, and plasticity

Project description:The hemochorial placenta provides a critical barrier at the maternal-fetal interface to modulate maternal immune tolerance and enable gas and nutrient exchange between mother and conceptus. Pregnancy outcomes are adversely affected by gestational diabetes mellitus (GDM); however, the effects of GDM on placental formation, and subsequently fetal development, are not fully understood. In this report, streptozotocin was used to induce hyperglycemia in pregnant rats for the purpose of investigating the impact of GDM on placental formation and fetal development. GDM caused placentomegaly and placenta malformation, decreasing placental efficiency and fetal size. Elevated glucose disrupted rat trophoblast stem (TS) cell differentiation in vitro. Evidence of altered trophoblast differentiation was also observed in vivo, as hyperglycemia affected the junctional zone transcriptome and interfered with intrauterine trophoblast invasion and uterine spiral artery remodeling. When exposed to hypoxia, rats with GDM showed decreased proliferation and ectoplacental cone development on gestation day (gd) 9.5 and complete pregnancy loss by gd 13.5. Furthermore, elevated glucose concentrations inhibited TS cell responses to hypoxia in vitro. Overall, these results indicate that alterations in placental development, efficiency, and plasticity could contribute to the suboptimal fetal outcomes in offspring from pregnancies complicated by GDM.

2020-07-07 | GSE144276 | GEO

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.

2018-08-01 | GSE106099 | GEO

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

2018-08-01 | GSE103552 | GEO

Offspring Sex Affects Placental DNA Methylation and Gene Expression in Diabetics

Project description:<p>Exposure to diabetes in utero is known to increase the offspring's likelihood of developing metabolic disease in adulthood, but the mechanisms involved are unknown. It has been proposed that early exposure to hyperglycemia and elevated insulin levels may lead to malprogramming of the fetus leading to the subsequent development of diabetes and obesity. Epigenetic modifications of the genome including DNA methylation, provide a plausible mechanism that allows for permanent propagation of gene activity states from one generation of cells to the next. </p> <p>The placenta, a fetal tissue easily accessible for study, is a complex organ that is essential in regulating fetal growth. The changes in placental nutrient transport associated with diabetes during pregnancy (DDP) have significant effects on the developing fetus, indicating that the placenta plays a critical role in fetal programming. The aim of our study was to investigate whether exposure to DDP alters genome-wide DNA methylation in the placenta obtained from term pregnancies resulting in differentially methylated loci of metabolically relevant genes and downstream changes in RNA and protein expression.</p>

| phs001535 | dbGaP

Human Placental Exosomes in Gestational Diabetes Mellitus Carry a Specific Set of miRNAs Associated with Skeletal Muscle Insulin Sensitivity

Project description:The objective of this study was to investigate whether placental exosomes in gestational diabetes mellitus (GDM) carries a specific set of miRNAs associated with skeletal muscle insulin sensitivity. Exosomes were isolated from chorionic villi-conditioned media and plasma from normal and GDM pregnancies. A specific set of miRNAs was identified to be selectively enriched within exosomes when compared to their cells of origin indicating specific packaging of miRNAs into exosomes. In addition, miRNA expression varies in a consistent pattern in placenta, placental-derived exosomes, circulating exosomes and skeletal muscle in GDM.

2021-03-20 | GSE112168 | GEO

miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

Project description:We report that the effect of GDM on gene expression differs between feto-placental endothelial cells of male vs female progeny, i.e. after pregnancy with a male or female offspring.

2019-01-01 | GSE104297 | GEO

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

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. 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

2015-08-03 | E-GEOD-70453 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data