Maternal-diabetes induced gene expression changes in the umbilical cord
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51546 | GEO | 2016/01/01
SECONDARY ACCESSION(S): PRJNA223401
REPOSITORIES: GEO
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Project description:Analysis of umbilical cord tissue in newborns of type 1 diabetic mothers at gene expression level. The hypothesis tested in the present study was that intrauterine diabetic milieu may effect of fetal umbilical cord gene expression, and via umbilical cord, the alterations may be produced in other fetal tissues as well. Results provide an information of the differentially expressed genes and enriched pathways, such as the dowregulated genes on the pathway on blood vessel development in umbilical cords from diabetic pregnancies. Umbilical cord tissue was collected after elective ceasarean section and was immediately flash frozen in liquid nitrogen and stored at -80C until total RNA extraction from the whole tissue sample. Six cords exposed to maternal diabetes (DM) and six control cords (C) from healthy pregnancies were analyzed.
2016-07-03 | E-GEOD-51546 | biostudies-arrayexpress
Project description:The discovery of fetal mRNA transcripts in maternal circulation holds great promise for noninvasive prenatal diagnosis. To identify potential fetal biomarkers, we studied whole blood and plasma transcripts common to term pregnant women and their newborns but reduced or absent in the postpartum mothers. In whole blood, 157 potentially-fetal transcripts were identified. RT-PCR confirmed the presence of specific transcripts, SNP analysis confirmed the presence of fetal transcripts in maternal circulation. Comparison of whole blood and plasma samples from the same women suggested that placental genes are more easily detected in plasma. We conclude that fetal and placental mRNA circulates in the blood of pregnant women. [I] We profiled whole antepartum (A), postpartum (P), and umbilical cord (U) blood samples from each of 9 mothers and their 10 newborns (1 set of twins, denoted as a and b after the sample names). [II] We also profiled plasma samples (A, P, and U) from three of those mothers to allow for a direct comparison between blood and plasma.
2014-01-08 | E-GEOD-53669 | biostudies-arrayexpress
Project description:Alteration of fetal kidney morphogenesis in diabetic pregnancies is poorly described, especially changes in the extracellular matrix (ECM) and glomerular basement membrane (GBM) during glomerulogenesis. Addressing the ECM proteome, or matrisome, in mouse fetal glomeruli in a healthy and diabetic environment will improve understanding about the association between ECM and GBM changes in the glomerulus as potential reprogramming mechanisms for glomerular dysfunction in infants of mothers with diabetes. This project aimed to define the matrisome and BM composition in the maturing murine fetal glomeruli collected from normal and diabetic mothers. For this, we used laser microdissection microscopy to isolate maturing glomeruli from cryosections, and analyse by label-free tandem mass spectrometry to test the hypothesis that maternal diabetes influences ECM and GBM composition, assembly and function.
2021-10-13 | PXD025911 | Pride
Project description:Intrauterine growth restriction (IUGR) is associated with increased susceptibility to obesity, metabolic syndrome and type 2 diabetes. Although the mechanisms underlying the fetal origin of metabolic disease are poorly understood, evidence suggests epigenomic alterations play a critical role. We sought to identify changes in DNA methylation patterns that define IUGR in CD3+ T-cells purified from umbilical cord blood obtained from appropriate for gestational age (Control) and IUGR male newborns using a genome-wide assay. We identified a global shift towards hypermethylation in IUGR compared to Control newborns targeted to regulatory regions of the genome.
2019-01-25 | GSE77268 | GEO
Project description:Primary endothelial cells from umbilical cord vein (HUVEC) obtained at delivery from gestational diabetic (GD) women, represent an expedient model for the study of the effects of chronic HG in vivo. In fetal tissues genome-wide epigenetic changes are likely to occur with specific long term and even trans-generational effects. We have utilized this model to study the effects of chronic hyperglycemia on the transcriptome and to verify the presence of specific epigenetic changes associated to chronic HG in vascular cells. HUVEC cells from Umbilical cords of 3 Caucasian Gestational Diabetes women were compared with HUVEC cells from umbilical of from 3 Caucasian non diabetic women matching for age and Body Mass Index. [sample collection] Umbilical cords were obtained from 3 Caucasian Gestational diabetes women (diagnosed not later than 28 th gestational week - gw) and from 3 Caucasian non diabetic women matching for age and Body Mass Index (BMI). All pregnants signed an informed consent. All donors were normotensive, and underwent a 100 g 3 hours Oral Glucose Tolerance Test (OGTT) between the 24 -34th gw. Each woman performed a 7 points-blood glucose monitoring on 3 days at week 34 -36th gw.
2013-08-08 | E-GEOD-49524 | biostudies-arrayexpress
Project description:Able to seqence microRNA from 2 x 6 mm dired blood spot chads from the BIBINS study. Samples are from newborns with moderate-severe HIE undergoing therapeutic hypothermia at around 16-24 h post insult, mild HIE without therapeutic hypothermia, and umbilical cord blodd from normal pregnancies.
2021-08-05 | GSE181127 | GEO
Project description:Fetal progenitor endothelial cells (endothelial colony forming cells; ECFC) are recruited for repair, vascular growth and angiogenesis and their high abundance perinatally suggests a function in postnatal vasculogenesis and angiogenesis. In this study we profiled ECFCs from pregnancies of control, overweight and diabetic mothers to study if adverse pregnancies are associated with epigenetic variation in ECFCs.
2021-12-14 | GSE180355 | GEO
Project description:Background: Maternal smoking during pregnancy is a major risk factor for adverse health outcomes. The main objective of the study was to assess the impact of in utero tobacco exposure on DNA methylation in children born at term with appropriate weight at birth. Methods: Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood (for methylation arrays) and maternal peripheral venous blood (for cotine level measurement) were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood. Results: The maternal plasmatic cotinine levels ranged from 10.70-115.40 ng/ml in the exposed group to 0-0.59 ng/ml in the non-exposed group. After adjusting for multiple comparisons in 427102 probes, statistically significant differences for 31 CpG sites, associated to 25 genes were observed. There was a greater than expected proportion of statistically-significant loci located in CpG islands (FisherM-bM-^@M-^Ys exact test, p=0.029) and of those CpG islands, 90.3% exhibit higher methylation levels in the exposed group. The most striking and significant CpG site, cg05727225, is located in the chromosome 11p15.4, within the adrenomedullin gene. Conclusions: In utero tobacco exposure, even in the absence of fetal growth restriction, may alter the epigenome, contributing to global DNA hypomethylation. Therefore, DNA status can be used as a biomarker of prenatal insults. Considering the possibility to reverse epigenetic modifications, a window of opportunity exists to change the programmed chronic disease. Twenty mother-newborn dyads, after uncomplicated pregnancies, in the absence of perinatal illness were included. All mothers were healthy with no cardiovascular risk factors, except for the associated risks among those mothers who smoked. Umbilical cord blood were collected and an epigenome-wide association study was performed using a 450K epigenome-wide scan (Illumina Infinium HumanMethylation 450BeadChip) with adjustment to normalize the DNA methylation for data cell variability in whole blood.
2015-02-16 | E-GEOD-64316 | biostudies-arrayexpress
Project description:During the COVID-19 pandemic, thousands of pregnant women have been infected with SARS-CoV-2 worldwide. The short- and long-term implications of maternal SARS-CoV-2 infection on fetal and childhood well-being are unknown. To characterize the fetal immune response to maternal SARS-CoV-2 infection, we performed single-cell RNA sequencing and T cell receptor sequencing on cord blood mononuclear cells from infants born to mothers infected with SARS-CoV-2 in the third trimester. We identified widespread gene expression changes in cord blood leukocytes, including upregulation of interferon-stimulated genes (ISG) and of HLA genes in CD14+ monocytes; decreased activation of CD16+ monocytes; activation of plasmacytoid dendritic cells; and activation and exhaustion of NK cells and T CD8+ cells in the cord blood of infants born to SARS-CoV-2+ mothers. Lastly, we observed fetal TCR repertoire clonal expansion in cord blood T cells from pregnancies complicated by maternal SARS-CoV-2 infection. Our results suggest that even in the absence of vertical transmission, SARS-CoV-2 maternal infection in the third trimester modulates the fetal immune system.
2021-04-06 | GSE165193 | GEO
Project description:Pregnant women and their fetuses are particularly susceptible to respiratory pathogens. How they respond to SARS-CoV-2 infection is still under investigation. Here, we studied the transcriptome and phenotype of umbilical cord blood cells in pregnant women infected or not with SARS-CoV-2. We found that symptomatic maternal COVID-19 was associated with a transcriptional erythroid cell signature as compared with asymptomatic and uninfected mothers. We observed an expansion of fetal hematopoietic progenitors skewed towards erythroid differentiation and displaying increased clonogenicity. We found no difference in inflammatory cytokines in the cord blood upon SARS-CoV-2 infection. Interestingly, we showed an activation of hypoxia pathway in cord blood cells from symptomatic COVID-19 mothers, suggesting that maternal hypoxia may be triggering this fetal stress erythropoiesis. Overall, these results show a fetal hematopoietic response to symptomatic COVID-19 in pregnant mothers in the absence of vertically transmitted SARS-CoV-2 infection, which is likely to be a mechanism of fetal adaptation to maternal infection and reduced oxygen supply.
2023-08-10 | GSE224063 | GEO