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Gene expression profiles in the PhIP/DSS-induced mouse colon tumors and the adjacent normal epithelium controls

ABSTRACT: Gene expression profiles in the PhIP/DSS-induced mouse colon tumors and the adjacent normal epithelium controls

PROVIDER: PRJNA565029 | ENA |

REPOSITORIES: ENA

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Gene expression profiles in the PhIP/DSS-induced mouse colon tumors and the adjacent normal epithelium controls

Project description:Differentially expressed genes in the PhIP/DSS-induced mouse colon tumors were identified through the mRNA expression profiles of the tumors and the matching controls using the mouse exonic evidence based oligonucleotide (MEEBO) microarray.

2019-09-12 | GSE137292 | GEO

Gene expression profiles of mouse colitis epithelial tissues induced by DSS or DSS/PhIP

Project description:We reported the gene expression profiles of hCYP1A mouse colitis epithelial tissues on Day 1, 3 and 7 after the treatment with DSS or DSS/PhIP for 5 days.

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Gene expression profiles of mouse colitis epithelial tissues induced by DSS or DSS/PhIP

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Expression data from colon epithelium of STAT3IEC-KO in acute DSS colitis

Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days

2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress

H3K27ac profiling in control and DSS-treated colonic epithelium

Project description:We determined changes in enhancer chromatin that occur during colonic inflammation, found that dynamic chromatin regions are enriched for HNF4A binding motirfs, and then measured HNF4A binidng by ChIP-seq in each condition. Examination of H3K27ac histone modification in normal and DSS-treated colon, examination of HNF4A binding by ChIP-seq in normal and DSS-treated colon epithelium

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RNA-seq in scraped colon epithelium after deletion of Synbindin in mice in colitis-associated cancer model

Project description:We previously identified Synbindin promoted gastric and colon cancer development by activating ERK on the Golgi in vitro. Advanced in vivo evidence is required.In this study, we genetically manipulated Synbindin expression in the intestinal epithelium using loss-of-function mouse models and subject them to AOM/DSS induced colitis-associated cancer model. At the end of the model, mice were sacrificed and colon tumors and adjacent colon epithelium were scraped and used for RNA-seq.

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PHIP occupancy in THP1 human AML cell line

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

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Expression profile of colon crypts from WT and GMCSF-/- mice with or without DSS treatment

Project description:To discover possible molecular mechanisms mediated by GM-CSF that may be involved in regeneration of the colon epithelium after DSS-induced injury we performed whole-genome wide mRNA microchip analysis of isolated crypt epithelial cells from unchallenged and DSS-challenged WT and GM-CSF-/- mice. Total RNA was prepared from isolated crypts obtained from colons of GM-CSF deficient mice and WT littermates treated or untreated with 1.5%DSS for 6 days. Three biological replicates were performed for each experimental condition.

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Defining the molecular properties of the repairing epithelium during DSS induced colitis

Project description:In order to understand the molecular changes associated with the establishment of the repairing epithelium following dextran sulfate sodium (DSS) induced injury of the colon we have isolated Epcam+Sca1+ expressing epithelial cells from repairing tissue and Epcam+ homeostatic intestine. Cells isolated by flow cytometry were subjected to RNA extraction and analysed by expression analysis

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Healthy, adjacent normal and tumor colon cells

Project description:Healthy, adjacent normal and tumor colon cells

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