Role of human fetal membranes in xenobiotic metabolism and nutrient transport
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA850439 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19737700.fastq.gz | Fastqsanger.gz | |||
| SRR19737701.fastq.gz | Fastqsanger.gz | |||
| SRR19737702.fastq.gz | Fastqsanger.gz | |||
| SRR19737703.fastq.gz | Fastqsanger.gz | |||
| SRR19737704.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 25 |
Similar Datasets
Project description:This study characterized CYP450 and nutrient transport expression in human fetal membranes. RNA sequencing (RNA-Seq) of RNA derived from human placental and fetal membrane tissues and cells was done.
2022-08-05 | GSE206401 | GEO
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:Sterile inflammation of the fetal membranes is an indispensable event of normal parturition. However, triggers of the sterile inflammation are not fully resolved. Serum amyloid A1 (SAA1) is an acute phase protein produced primarily by the liver, which is believed to be implicated in the host inflammatory response to ensure early survival. Emerging evidence indicates that SAA1 can also be synthesized in extra-hepatic tissues including gestational tissues. Moreover, SAA1 synthesis is greatly enhanced in gestational tissues at parturition. Given the inflammatory actions of SAA1, we hypothesized that increased SAA1 synthesis locally in the fetal membranes may act as a humoral trigger of sterile inflammation of the fetal membranes at parturition. Here, by using transcriptomic sequencing and multiplex immunoassay, we found that multiple pathways related to chemotaxis were evoked by SAA1 in human amnion fibroblasts along with upregulation of a series of chemokines, particularly CCL3, CXCL6 and CCL20. Mechanistic studies showed that both toll-like receptor 4 (TLR4) and formyl peptide receptor 2 (FPR2) was involved in the induction of chemokines by SAA1. Moreover, SAA1-conditioned culture medium of amnion fibroblasts was capable of chemoattracting virtually all types of mononuclear leukocytes, particularly monocytes and dendritic cells, which reconciled well with the chemotactic activity of conditioned culture medium of amnion tissue explants collected from spontaneous labor. The infiltration of monocytes and dendritic cells to the fetal membranes at parturition was confirmed both morphologically with immunohistochemical staining and quantitatively with Western blotting. Additionally, SAA1 could also activate monocytes/macrophages and dendritic cells towards a proinflammatory phenotype. Conclusively, increased local SAA1 synthesis may trigger sterile inflammation of the fetal membranes at parturition by stimulating chemokine production initially in local cells resulting in increased chemotaxis of mononuclear leukocytes to the membranes to facilitate their transition towards the proinflammatory phenotype.
2025-11-10 | GSE217734 | GEO
Project description:Transcriptomic analysis delineates preterm prelabor rupture of membranes from preterm labor in preterm fetal membranes
| PRJNA1020124 | ENA
Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition
| PRJNA700435 | ENA
Project description:We have developed a baboon nonhuman primate (NHP) model of maternal nutrient reduction during fetal development (30% global maternal nutrient reduction, MNR) to evaluate the impact of reduced nutrient availability on primate fetal development. We reported (Antonow-Schlorke et al. PNAS, 2011) that MNR induced major cerebral developmental disturbances at mid gestation (0.5G); however, the impact of MNR at late gestation (0.9G) and the mechanisms mediating these effects have not been determined. We hypothesized that MNR alters developmental trajectories of the fetal prefrontal cortex in the late gestation via miRNA regulation of key transcriptional and translational signaling pathways. Pregnant baboons were fed either ad libitum (control; CON; females n=3; males n=3) or a globally reduced diet (70% of controls; females n=3; males n=3) from 0.16G through 0.9G that produces IUGR (14% reduction in fetal weight). Fetuses were removed by Cesarean section at 0.9G, and prefrontal cortex (PFC) sections collected for analysis. Transcriptome (gene arrays) and small transcriptome (small RNA-Seq) analyses of fetal PFC were performed and gene and miRNA profiles were compared between MNR and CON. We present for the first time transcriptome (GSE42756) and small RNA transcriptome expression profiles of the fetal baboon PFC at 0.9G. Pathway analysis showed that MNR had sex-specific effects on key cellular signaling pathways. We conclude that moderate maternal global nutrient reduction during pregnancy can alter signaling pathways related to nutrient sensing and cell proliferation in the late gestation PFC. In addition, inverse expression of miRNAs known to target genes in these pathways suggests that miRNA mechanisms play a role in these changes.
2018-09-03 | GSE61213 | GEO
Project description:Despite the documented benefits of breastfeeding and major governmental advocacy efforts, a paucity of data exists regarding the transfer of most drugs into breast milk. Passive diffusion governs the extent of accumulation for most drugs and the exposure risk can therefore be predicted using mathematical models. However, examples of xenobiotic accumulation into breast milk well above that predicted by passive diffusion have been documented and attributed to drug transport. A thorough evaluation of the expression of xenobiotic transporters in mammary epithelial cells (MECs), the cells that form the anatomical barrier between maternal serum and breastmilk, during lactation is necessary to determine the drugs for which an active transport mechanism governs transfer into breast milk and to improve predictive models. We used microarrays to evaluate gene expression in human mammary epithelial cells and identified xenobiotic trasnporter genes that were upregulated during lactation.
2017-07-01 | GSE18287 | GEO
Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition [ChIP-seq]
| PRJNA700988 | ENA