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:Role of human fetal membranes in xenobiotic metabolism and nutrient transport
| PRJNA850439 | ENA
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: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: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:Transcriptomic analysis delineates preterm prelabor rupture of membranes from preterm labor in preterm fetal membranes
| PRJNA1020124 | ENA
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: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:C/EBPδ drives key endocrine signals in human fetal membranes at parturition [RNA-seq]
| PRJNA700987 | ENA
Project description:Altered metabolism, such as aerobic glycolysis or the Warburg effect, has been recognized as characteristics of tumor cells for almost a century. Since then, there is accumulating evidence to demonstrate the metabolic reprogramming of tumor cells, addiction to excessive uptake and metabolism of key nutrients, to support rapid proliferation and invasion under tumor microenvironment. The solute carrier (SLC) superfamily transporters are responsible for influx or efflux of a wide variety of xenobiotic and metabolites that are needed for the cells to function, as well as some medications. To meet the increased demand for nutrients and energy, SLC transporters are frequently dysregulated in cancer cells. The SLCs responsible for the transport of key nutrients for cancer metabolism and energetics, such as glucose and amino acids, are of particular interest for their roles in tumor progression and metastasis. Meanwhile, rewired metabolism is accompanied by the dysregulation of microRNAs (miRNAs or miRs) that are small, noncoding RNAs governing posttranscriptional gene regulation. Studies have shown that many miRNAs directly regulate the expression of specific SLC transporters in normal or diseased cells. Changes of SLC transporter expression and function can subsequently alter the uptake of nutrients or therapeutics. Given the important role for miRNAs in regulating disease progression, there is growing interest in developing miRNA-based therapies, beyond serving as potential diagnostic or prognostic biomarkers. In this article, we discuss how miRNAs regulate the expression of SLC transporters and highlight potential influence on the supply of essential nutrients for cell metabolism and drug exposure toward desired efficacy.
| S-EPMC9220936 | biostudies-literature
Project description:Reverse Osmosis Membranes Fractions Raw sequence reads
| PRJNA629347 | ENA