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Role of human fetal membranes in xenobiotic metabolism and nutrient transport

ABSTRACT: Role of human fetal membranes in xenobiotic metabolism and nutrient transport

PROVIDER: PRJNA850439 | ENA |

REPOSITORIES: ENA

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			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

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Role of human fetal membranes in xenobiotic metabolism and nutrient transport

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.

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Expression data from fetal membranes

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.

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Transcriptomic analysis delineates preterm prelabor rupture of membranes from preterm labor in preterm fetal membranes

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.

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Transcriptomic Profiling of Fetal Membranes of Mice Deficient in Biglycan and Decorin as a Model of Preterm Birth

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.

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Transcriptomic analysis delineates preterm prelabor rupture of membranes from preterm labor in preterm fetal membranes

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C/EBPδ drives key endocrine signals in human fetal membranes at parturition

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Discovery of canonical and non-canonical miRNAs in brain frontal cortex in control and maternal nutrient restricted fetal baboon

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.

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Xenobiotic transporter gene expression in isolated lactating and non-lactating human mammary epithelial cells

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Project description:C/EBPδ drives key endocrine signals in human fetal membranes at parturition [ChIP-seq]

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