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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide Profiling of NR2F2 (COUP-TFII) Binding in Human Endometrial Stromal Cells [ChIP-Seq]

ABSTRACT: ChickenM-BM- ovalbumin upstream promoter-transcription factor II (COUP-TFII; NR2F2) is an orphan nuclear receptor involved in cell-fate specification, organogenesis, angiogenesis and metabolism. Ablation of COUP-TFII in the mouse uterus causes infertility due to defects in embryo attachment and impaired uterine stromal cell decidualization. Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown. To better elucidate the mechanisms with which COUP-TFII regulates target gene transcription, genome-wide COUP-TFII binding sites in human endometrial stromal cells (HESC) treated with deciduogenic hormones were identified using ChIP-seq. A total of 16,298 intervals (binding regions) for COUP-TFII were identified compared with the input in HESC chromatin with a very low false discovery rate (0.17%) using a stringent cutoff of p =1x10-10. Distribution of intervals showed that more than half (58.6%) of the COUP-TFII binding sites are located within 10 kb of gene boundaries. 7.5% of total intervals reside within the 10 kb promoter region. A total of 6,077 unique genes were identified to have COUP-TFII binding sites within 10 kb of their gene boundaries. Examination of NR2F2 binding in pooled primary human endometrial stromal cells from 6 healthy women upon decidualization with a hormone cocktail of cAMP, E2 and medroxyprogesterone acetate.

ORGANISM(S): Homo sapiens

SUBMITTER: Francesco DeMayo

PROVIDER: E-GEOD-52008 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide Profiling of NR2F2 (COUP-TFII) Binding in Human Endometrial Stromal Cells [ChIP-Seq]

Project description:Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII; NR2F2) is an orphan nuclear receptor involved in cell-fate specification, organogenesis, angiogenesis and metabolism. Ablation of COUP-TFII in the mouse uterus causes infertility due to defects in embryo attachment and impaired uterine stromal cell decidualization. Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown. To better elucidate the mechanisms with which COUP-TFII regulates target gene transcription, genome-wide COUP-TFII binding sites in human endometrial stromal cells (HESC) treated with deciduogenic hormones were identified using ChIP-seq. A total of 16,298 intervals (binding regions) for COUP-TFII were identified compared with the input in HESC chromatin with a very low false discovery rate (0.17%) using a stringent cutoff of p =1x10-10. Distribution of intervals showed that more than half (58.6%) of the COUP-TFII binding sites are located within 10 kb of gene boundaries. 7.5% of total intervals reside within the 10 kb promoter region. A total of 6,077 unique genes were identified to have COUP-TFII binding sites within 10 kb of their gene boundaries.

2013-11-02 | GSE52008 | GEO

Orphan nuclear receptor COUP-TFII enhances myofibroblasts glycolysis leading to kidney fibrosis

Project description:Recent studies demonstrated that metabolic disturbance, such as augmented glycolysis, contributes to fibrosis. The molecular regulation of this metabolic perturbation in fibrosis, however, has been elusive. COUP-TFII (also known as NR2F2) is an important regulator of glucose and lipid metabolism. Its contribution to organ fibrosis is undefined. Here, we found increased COUP-TFII expression in myofibroblasts in human fibrotic kidneys, lungs, kidney organoids, and mouse kidneys after injury. Genetic ablation of COUP-TFII in mice resulted in attenuation of injury-induced kidney fibrosis. A non-biased proteomic study revealed the suppression of fatty acid oxidation and the enhancement of glycolysis pathways in COUP-TFII overexpressing fibroblasts. Overexpression of COUP-TFII in fibroblasts induced augmented glycolysis and production of alpha smooth muscle actin (αSMA) and collagen1. Knockout of COUP-TFII decreased glycolysis and collagen1 levels in fibroblasts. Chip-qPCR revealed the binding of COUP-TFII on the promoter of PGC1α. Overexpression of COUP-TFII reduced the cellular level of PGC1α. Targeting COUP-TFII serves as a novel treatment approach for mitigating fibrosis in chronic kidney disease and potentially fibrosis in other organs.

2021-04-27 | PXD024035 | Pride

COUP-TFII regulates human endometrial stromal genes involved in inflammation

Project description:Although the function of COUP-TFII in uterine decidualization has been described in mice, its role in the human uterus remains unknown.To interrogate the role of COUP-TFII in human endometrial function, we utilized a siRNA-mediated loss of function approach in primary human endometrial stromal cells. Primary human endometrial stromal cells (HESCs), coup-TFII siRNA group and control group Two group comparison

2014-01-07 | E-GEOD-47052 | biostudies-arrayexpress

Atrial Identity Is Determined by A COUP-TFII Regulatory Network (ChIP-Seq)

Project description:Embryonic cardiomyocytes possess the plasticity to choose between atrial and ventricular fates. For a limited window of time, the transcription factor COUP-TFII (Nr2f2) sufficiently and essentially confers the atrial identity through direct and indirect regulation of nearly half of chamber specific genes. Examination of COUP-TFII binding sites in embryonic artia

2013-06-07 | E-GEOD-46497 | biostudies-arrayexpress

Microarray analysis of mRNA expression in E14.5 and E16.5 mouse ovaries with and without Coup-tfII (Nr2f2)

Project description:COUP-TFII (NR2F2) is expressed in somatic cells in fetal ovary. To investigate the function of COUP-TFII , we used Cre-flox model to ablate Coup-tfII in the fetal ovaries We performed microarray to compare gene expression profile between control and knockout ovaries.

2018-01-12 | GSE100015 | GEO

COUP-TFII regulates human endometrial stromal genes involved in inflammation

2014-01-07 | GSE47052 | GEO

Atrial Identity Is Determined by A COUP-TFII Regulatory Network (ChIP-Seq)

2013-06-07 | GSE46497 | GEO

Genome-wide binding sites of COUP-TFII in the E14.5 mesonephroi

Project description:In an XX embryo, the Wolffian duct regresses under the control of the mesenchymal transcription factor COUP-TFII. To understand cellular and molecular actions underlying Wolffian duct regression, we preformed transcriptomic analyses of XX mesonephroi with or without Coup-tfII and genome-wide analysis of COUP-TFII chromatin occupancy in XX mesonephroi. The integrative analysis of COUP-TFII genome-wide binding and transcriptomic analysis revealed the suppression of muscle differentiation and extracellular matrix genes by COUP-TFII and identified a group of COUP-TFII’s potential transcriptional partners in the mesenchyme that potentially facilitate Wolffian duct regression. These findings provide insights into the molecular action of COUP-TFII in the Wolffian duct mesenchyme and identify a list of biologically relevant candidate genes and pathways for future functional analyses in sexual differentiation of reproductive tracts.

2022-04-20 | GSE157836 | GEO

Expression data from control and COUP-TFII siRNA treated PC3 cells

Project description:COUP-TFII, a member of the nuclear receptor superfamily plays a critical role in angiogenesis and organogenesis during embryonic development. Our results indicate that COUP-TFII expression is profoundly upregulated in prostate cancer patients and might serves as biomarker for recurrence prediction. Thus we conduct transcriptome comparison of control and COUP-TFII depleted PC3 cells to gain genomic insights on the biological processes that COUP-TFII is involved in prostate cancer cells. Ingenuity Pathway Analysis (IPA) shows that the most prominent altered pathways in the COUP-TFII depleted cells are related to cell growth; cell cycle progression and DNA damage response. Indeed many growth related genes including E2F1, p21, CDC25A, Cyclin A and Cyclin B are changed in COUP-TFII knockdown cells, suggesting that COUP-TFII might be an important regulator for prostate cancer cell growth. Further functional assays from cells and mice genetic studies confirm the hypothesis that COUP-TFII serve as the major regulator to control prostrate cancer growth. Together, results provide insight into the role of COUP-TFII in prostate tumorigenesis.

2011-10-25 | GSE33182 | GEO

Expression data from control and COUP-TFII siRNA treated HUVEC cells

Project description:COUP-TFII plays a critical role in angiogenesis during development. It has also been shown to suppress Notch signaling pathway to confer vein identity. However, the downstream targets and the mechanism mediate COUP-TFII function to regulate these processes remain elusive. To identify the downstream targets and the mechanism by which COUP-TFII regulates agiogenesis and vein specification, we knocked down COUP-TFII in HUVEC cells using COUP-TFII specific siRNA and used microarray analysis to identify downstream targets. Interestingly, we found the expression of many genes in the cell cycle pathway and Notch signaling pathway are significantly altered in the COUP-TFII depleted cells.

2011-10-28 | GSE33301 | GEO

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