Role of human fetal membranes in xenobiotic metabolism and nutrient transport
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE206401 | GEO | 2022/08/05
REPOSITORIES: GEO
Similar Datasets
Project description:Genome wide expression profiling was used to identify signifnificantly changed genes in fetal membranes after GBS treatment Genome-wide expression profiles in GBS-inoculated human extraplacental membranes in vitro were used to identify transcriptomic pathways altered by GBS . Using bioinformatics analysis of these expression profiles we aimed to test our hypothesis that GBS activates pathways related to inflammation and premature birth in human extraplacental membranes.
2018-01-18 | GSE96557 | GEO
Project description:We compared fetal membrane tissue from preterm labor deliveries to fetal tissue from preterm labor with preterm prelabor rupture of membranes (PPROM) deliveries to further explore the concept that spontaneous preterm birth can result from the initializing of two separate but overlapping pathological events. Chorioamnion, separated into amnion and chorion, was collected from gestationally age-matched cases and controls within 15 minutes of birth, and analyzed using RNA sequencing. In our study, transcriptome analysis of preterm fetal membranes revealed distinct differentially expressed genes for PPROM, separate from preterm labor. This study is the first to report transcriptome data that reflects the individual pathophysiology of amnion and chorion tissue from PPROM deliveries.
2024-03-13 | GSE243831 | GEO
Project description:Approximately 25% of all preterm births are due to preterm premature rupture of membranes. Mice deficient in proteoglycans biglycan (Bgn) and decorin (Dcn) display abnormal fetal membranes and increased incidence of preterm birth. We conducted RNA-Seq to profile fetal membranes and identify molecular pathways that may lead to preterm birth in double knockout (DKO) mice (Bgn −/−; Dcn −/− ) compared to wild-type (WT) at two different gestational stages, E12 and E18 (n=3 in each group). 3264 transcripts were differentially regulated in E18 DKO vs. WT fetal membranes, and 96 transcripts differentially regulated in E12 DKO vs. WT fetal membranes (FDR<0.05, log 2 FC≥1). Differentially regulated transcripts in E18 DKO fetal membranes were significantly enriched for genes involved in cell cycle regulation, extracellular matrix-receptor interaction, and the complement cascade. 50 transcripts involved in the cell cycle were altered in E18 DKO fetal membranes (40↓, 10↑, FDR<0.05), including p21 and p57 (↑), and Tgfb2, Smad3, CycA, Cdk1, and Cdk2(↓). Thirty-one transcripts involved in the complement cascade were altered (11↓, 20↑, FDR<0.05) in E18 DKO fetal membranes, including C1q, C2, and C3 (↑). Differentially expressed genes in the top three molecular pathways (1) showed evidence of negative or purifying selection, and (2) were significantly enriched (Z-score>10) for transcription factor binding sites for Nr2f1 at E18. We propose that in DKO mice, cell cycle arrest results in lack of cell proliferation in fetal membranes, inability to contain the growing fetus, and preterm birth.
2020-12-03 | GSE162502 | GEO
Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition [RNA-seq]
| PRJNA700987 | ENA
Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition
| PRJNA700435 | ENA
Project description:Acute chorioamnionitis (aCA) is a commonly reported histologic lesion in at least 40% of spontaneous preterm deliveries. It is typically characterized by an infiltration of maternal neutrophils into the chorioamniotic membranes and is also associated with other placental inflammatory lesions such as acute intervillositis and acute villitis. DNA methylation (DNam) is an easily measurable epigenetic mark, which is more stable than mRNA. While DNAm may influence gene expression in specific cell types, it may also reflect altered cell composition. Studies have previously documented aCA-associated cellular changes primarily in the context of a polymicrobial invasion of the amniotic space. We, thus hypothesize that changes in DNAm associated with aCA will occur predominantly as a consequence of the response to infection, in particular due to alterations in the number of neutrophils and/or other alterations in cell populations inherent to the placenta. Pooled chorionic villus samples (22 aCA cases, 22 non-aCA cases) and fetal membranes (amnion and chorion) (9 aCA cases, 7 non-aCA cases) were evaluated using the Illumina EPIC array, which quantifies DNAm at >850,000 sites in the genome. We identified 66 differentially methylated sites associated with aCA (FDR <0.15, methylation difference >0.05). At the same thresholds, ~20% chorionic villi sites were also differentially methylated in chorion, but none were observed in amnion. Using publicly available datasets, we identified 2069 neutrophil-specific CpGs by differential methylation analysis. Euclidean clustering of our chorionic villi DNAm data (n=44 samples) using 2069 neutrophil-specific CpG sites largely separated aCA cases from the non-aCA cases, suggesting activation of innate immune responses in aCA-associated placentas.
2018-11-06 | GSE115508 | GEO
Project description:A family of vertebrate-specific microRNAs called the ESCC microRNAs regulates proliferation and differentiation of embryonic stem cells. The ESCC microRNAs arise from two genetic loci in mammals, the miR-290/miR-371 and miR-302 loci. While the miR-302 locus is found broadly among vertebrates, the miR-290/miR-371 locus is unique to eutherian species, suggesting a role in placental development. Here, we evaluate that role. A knockin reporter for the mouse miR-290 gene is expressed throughout the embryo until gastrulation, at which time it becomes specifically expressed in extraembryonic tissues and the germline. In the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed until birth. Deletion of the miR-290 gene results in reduced trophoblast progenitor cell proliferation and a reduced DNA content in endoreduplicating trophoblast giant cells. A reduction in placental size precedes a reduction in fetal size and prenatal death of most knockout embryos. The vascular labyrinth shows disorganization with thickening of the barrier between maternal and fetal blood associated with reduced diffusion of a radioactive tracer. Multiple mRNA targets of the cluster miRNAs are upregulated. Together, these data uncover a critical function for the miR-290 in the regulation of a network of genes required for normal placental development, suggesting a central role for this microRNA cluster in the evolution of eutherian species.
2017-03-04 | GSE95687 | GEO
Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition [ChIP-seq]
| PRJNA700988 | ENA
Project description:We sought to identify changes in placental gene expression that may contribute to the phenotype of NDRG1-deficient embryos, and to define the contribution of hypoxia and fetal sex to these changes. We therefore used high-density oligonucleotide microarrays to interrogate differences in placental gene expression, stratified by fetal sex, Ndrg1 status (WT vs KO) and oxygenation (21% vs 12%). C57Bl6/J mice heterozygous for NDRG1-null allele were bred and separated next day (E0.5), and give ad libitum access to standard chow and water with 12h light:dark cycle. Pregnant dams were sacrificed at E15.5 by cervical dislocation following isoflurane anesthesia. Following sacrifice, embryos and placentas were collected, NDRG1 genotype and sex were determined by PCR of fetal tissue, and RNA was extracted from placental tissue following removal of membranes.
2013-04-26 | E-GEOD-46381 | biostudies-arrayexpress
Project description:Maternal influenza A viral infections in humans are associated with low birth weight, increased risk of pre-term birth, stillbirth and congenital defects. To examine the effect of maternal influenza virus infection on placental and fetal growth, pregnant C57BL/6 mice were inoculated intranasally with influenza A virus A/CA/07/2009 pandemic H1N1 or PBS at E3.5, E7.5 or E12.5, and the placentae and fetuses collecgted and weighed at E18.5. Fetal thymuses were pooled from each litter. Placentae were examined histologically, stained by IHC for CD34 and vascular channels quantified. RNA from E7.5 and E12.5 placentae and E7.5 fetal thymuses was subjected to RNA sequencing and pathway analysis. Placental weights were decreased in litters inoculated with influenza at E3.5 and E7.5. Placentae from E7.5 and E12.5 inoculated litters exhibited decreased labyrinth development and transmembrane protein 150A gene was upregulated in E7.5 placentae. Fetal weights were decreased in litters inoculated at E7.5 and E12.5 compared to controls. RNA sequencing of E7.5 thymuses indicated that 957 genes were downregulated 2-fold including Mal, which is associated with Toll-like receptor signaling and T cell differentiation. There were 28 upregulated genes. It is concluded that maternal influenza A virus infection impairs fetal thymic gene expression as well as restricting placental and fetal growth.
2020-09-11 | GSE157132 | GEO