Effect of chorioamnionitis exposure on neonatal monocyte transcription
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ABSTRACT:
PROVIDER: PRJNA438588 | ENA |
REPOSITORIES: ENA
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Project description:We sought to determine the impact of chorioamnionitis exposure on term neonatal monocyte transcription. RNA-seq was performed on term healthy and chorioamnionitis-exposed umbilical cord blood purified CD14+ monocytes under unstimulated and LPS stimulated conditions.
2018-08-01 | GSE111927 | GEO
Project description:We sought to determine the impact of chorioamnionitis exposure on the neonatal monocyte H3K4me3 histone modification landscape over the course of fetal and neonatal immune system development using ChIP-seq. H3K4me3 ChIP-seq was performed on umbilical cord blood purified CD14+ monocytes from healthy and chorioamnionitis-exposed extremely preterm neonates (under 30 weeks gestation), late preterm neonates (30-36 weeks gestation), and term neonates (37+ weeks gestation).
2018-08-01 | GSE111873 | GEO
Project description:Impact of chorioamnionitis exposure on neonatal monocyte H3K4me3 patterning
| PRJNA438452 | ENA
Project description:To identify candidate miRNAs in amniotic fluids as biomarkers for chorioamnionitis, we compared miRNA array data in amniotic fluids between pregnant women with the absence and presence of histological chorioamnionitis.
2021-02-01 | GSE143193 | GEO
Project description:We used single-nuclei sequencign to determine the effect of chorioamnionitis to the developing cerebellum using a rhesus macaque model of chorioamnionitis induced by intra-amniotic LPS.
2024-01-17 | GSE205001 | GEO
Project description:Preterm premature rupture of membranes (PPROM), which precedes approximately 30–40% of preterm births, is the main cause of neonatal morbidity, mortality, and long-term sequelae. In particular, almost half of all PPRPM cases are frequently complicated by subclinical acute inflammation in the placenta and fetal tissue, commonly named as acute histologic chorioamnionitis [HCA]. Increasing evidences suggest that HCA carries additional risks to both the pregnant women and their fetuses, including greater risk of imminent preterm birth, as well as sepsis, neurologic morbidity, and mortality in neonates. More accurate and early prenatal predictive markers (especially noninvasive ones) are urgently needed for identifying subclinical HCA in the context of PPROM.To identify potential biomarkers in the plasma that could predict histologic chorioamnionitis (HCA) in women with preterm premature rupture of membranes (PPROM), using shotgun and targeted proteomic analyses.
2022-08-12 | PXD027573 | Pride
Project description:Human transcriptome array analysis of human cord blood mononuclear leokocytes from neonates exposed to histological chorioamnionitis and compared with healthy neonates Histological chorioamnionitis (HCA) is an infection of fetal membranes and complicates 5.2% to 28.5% of all live births. Exposure to HCA may have long-term consequences including an increased risk for allergic disorders and asthma later in childhood, the mechanism(s) of which are still not yet well understood. Our objective was to determine the mRNA transcriptome of cord blood mononuclear leukocytes from term neonates and identify key genes and pathways involved in HCA. We found several key genes differentially expressed with exposure to HCA. These transcriptomes included novel genes and pathways associated with exposure to HCA. The differential gene expression included the key genes regulating inflammatory, immune, respiratory and neurological pathways, which may contribute to disorders in those pathways in neonates exposed to HCA.
2019-04-05 | GSE120855 | GEO
Project description:Newborns, particularly those born prematurely, are extremely vulnerable to sepsis and this has been attributed to ‘immature’ innate monocyte defences. Predominant pathogens include Escherichia. coli and Staphylococcus. epidermidis but no studies have assessed global transcriptional responses of neonatal monocytes to live sepsis-causing bacteria. Here, we aimed to identify and characterise the common and pathogen-specific, neonatal monocyte transcriptional responses to E. coli and S. epidermidis to better understand early life innate immune responses. RNA-sequencing was performed on purified cord blood monocytes from very preterm (<32 weeks gestational age, GA) and term infants (37-40 weeks GA) following standardised challenge with live S. epidermidis or E. coli.
2018-03-16 | GSE101880 | GEO
Project description:Developmental exposure to diethylstilbestrol (DES) causes reproductive tract malformations, affects fertility and increases the risk of clear cell carcinoma of the vagina and cervix in humans. Previous studies on a well-established mouse DES model demonstrated that it recapitulates many features of the human syndrome, yet the underlying molecular mechanism is far from clear. Using the neonatal DES mouse model, the present study uses global transcript profiling to systematically explore early gene expression changes in individual epithelial and mesenchymal compartments of the neonatal uterus. Over 900 genes show differential expression upon DES treatment in either one or both tissue layers. Interestingly, multiple components of the Peroxisome Proliferator-Activated Receptor gamma (PPAR gamma)-mediated adipogenic/lipid metabolic pathway, including PPARgamma itself, are targets of DES in the neonatal uterus. TEM and Oil Red O staining further demonstrate a dramatic increase in lipid deposition in the uterine epithelial cells upon DES exposure. Neonatal DES exposure also perturbs glucose homeostasis in the uterine epithelium. Some of these neonatal DES-induced metabolic changes appear to last into adulthood, suggesting a permanent effect of DES on energy metabolism in uterine epithelial cells. This study extends the list of biological processes that can be regulated by estrogen or DES, and provides a novel perspective for endocrine disruptor induced reproductive abnormalities.
2012-05-15 | GSE37969 | GEO
Project description:Developmental exposure to diethylstilbestrol (DES) causes reproductive tract malformations, affects fertility and increases the risk of clear cell carcinoma of the vagina and cervix in humans. Previous studies on a well-established mouse DES model demonstrated that it recapitulates many features of the human syndrome, yet the underlying molecular mechanism is far from clear. Using the neonatal DES mouse model, the present study uses global transcript profiling to systematically explore early gene expression changes in individual epithelial and mesenchymal compartments of the neonatal uterus. Over 900 genes show differential expression upon DES treatment in either one or both tissue layers. Interestingly, multiple components of the Peroxisome Proliferator-Activated Receptor gamma (PPAR gamma)-mediated adipogenic/lipid metabolic pathway, including PPARgamma itself, are targets of DES in the neonatal uterus. TEM and Oil Red O staining further demonstrate a dramatic increase in lipid deposition in the uterine epithelial cells upon DES exposure. Neonatal DES exposure also perturbs glucose homeostasis in the uterine epithelium. Some of these neonatal DES-induced metabolic changes appear to last into adulthood, suggesting a permanent effect of DES on energy metabolism in uterine epithelial cells. This study extends the list of biological processes that can be regulated by estrogen or DES, and provides a novel perspective for endocrine disruptor induced reproductive abnormalities. We separated UE from the UM from vehicle (oil)- or DES-treated postnatal day 5 (P5) mice, and prepared biological triplicates of RNA from pooled specimens (nM-bM-^IM-%3). Those samples were analyzed on two MouseWG-6 BeadChips, which detects 45,200 transcripts including more than 26,000 annotated genes in the NCBI RefSeq database. Difference of at least twofold in signal intensity of each given probe set with a P-value less than 0.05 was considered statistically significant.
2012-05-14 | E-GEOD-37969 | biostudies-arrayexpress