Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA179229 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To describe the protein profile in hippocampus, colon and ileum tissue’ changing after the old faeces transplants, we adopted a quantitative label free proteomics approach.
2021-09-09 | PXD016432 | Pride
Project description:Gene expression data from DSS-treated crypts, normal colon crypts and tumor crypts
| PRJNA242308 | ENA
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.
2012-11-21 | E-GEOD-42173 | biostudies-arrayexpress
Project description:Comparative gene expression profiling between DSS-treated crypts and normal colon crypts Comparative gene expression profiling between normal colon crypts and tumor crypts
2017-01-01 | GSE56050 | GEO
Project description:Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice are all more sensitive than wild type (WT) mice to dextran sulfate sodium (DSS)-induced colitis. The purpose of this study was to determine which genes are differentially induced by DSS treatment in the colon of Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice compared to WT mice. The results demonstrate higher induction of proinflammatory gene expression in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice than in WT mice after DSS treatment. The majority of genes whose expression is increased in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice but not in WT mice are interferon-inducible genes. Thus, Peptidoglycan Recognition Proteins Pglyrp1, Pglyrp2, Pglyrp3, and Pglyrp4 protect mice from excessive inflammatory response and damage to the colon by limiting expression of interferon-inducible genes in the colon.
2010-08-23 | GSE18859 | GEO
Project description:DIGE results of mouse models of colon cancer. Tissue harvested from small intestines of Apc1638N+/- and p21-/- mice as per the method developed by Wieser et al. (1973). Spots identified as significant (alpha<0.05) in the comparison of mutant mouse crypts and villi to WT crypts and villi, respectively.
2012-05-02 | PRD000177 | Pride
Project description:Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) that predisposes to colorectal cancer (CRC) and is modeled in mice by administration of dextran sodium sulfate (DSS) in drinking water. There are two isoforms of STAT3, STAT3α is pro-inflammatory and anti-apoptotic, while STAT3β has opposing effects on STAT3α. We examined the severity of DSS-induced colitis in transgenic-mice expressing only STAT3α ( / ) and in wild-type (WT) mice administered C188-9, a small molecule direct-inhibitor of STAT3. While manifestations of DSS-induced UC, such as mortality, weight-loss, rectal-bleeding, diarrhea, and colon-shortening, were exacerbated in / transgenic versus cage-control WT mice, all were prevented by C188-9 treatment of WT mice. C188-9 treatment also increased apoptosis of pathogenic CD4+T-cells, reduced colon-levels of IL17-positive cells, down-modulated mRNA-levels of STAT3-genes involved in inflammation, apoptosis-prevention, and colorectal-cancer-metastases. These are the only studies showing efficacy of Thus small-molecule targeting of STAT3 may be a useful novel approach in treating UC and preventing UC-associated colorectal-cancer. We performed genome-wide microarray expression profiling to gain greater understanding of the mechanisms involved in the protective effect of C188-9 in DSS-induced colitis, we examined mRNA levels in the colon of mice receiving DSS or plain water, without or with C188-9 treatment.
2019-07-24 | GSE117355 | GEO
Project description:Inflammatory bowel disease is characterized by chronic relapsing idiopathic inflammation of the gastrointestinal tract and persistent inflammation. Studies focusing on the immune-regulatory function of reactive oxygen species (ROS) are still largely missing. In this study, we analyzed an ROS-deficient mouse model leading to colon adenocarcinoma. Colitis was induced with dextran sulfate sodium (DSS) supplied via the drinking water in wild-type (WT) and Ncf1-mutant (Ncf1) B10.Q mice using two different protocols, one mimicking recovery after acute colitis and another simulating chronic colitis. Disease progression was monitored by evaluation of clinical parameters, histopathological analysis, and the blood serum metabolome using 1H nuclear magnetic resonance spectroscopy. At each experimental time point, colons and spleens from some mice were removed for histopathological analysis and internal clinical parameters. Clinical scores for weight variation, stool consistency, colorectal bleeding, colon length, and spleen weight were significantly worse for Ncf1 than for WT mice. Ncf1 mice with only a 7-day exposure to DSS followed by a 14-day resting period developed colonic distal high-grade dysplasia in contrast to the low-grade dysplasia found in the colon of WT mice. After a 21-day resting period, there was still β-catenin-rich inflammatory infiltration in the Ncf1 mice together with high-grade dysplasia and invasive well-differentiated adenocarcinoma, while in the WT mice, high-grade dysplasia was prominent without malignant invasion and only low inflammation. Although exposure to DSS generated less severe histopathological changes in the WT group, the blood serum metabolome revealed an increased fatty acid content with moderate-to-strong correlations to inflammation score, weight variation, colon length, and spleen weight. Ncf1 mice also displayed a similar pattern but with lower coefficients and showed consistently lower glucose and/or higher lactate levels which correlated with inflammation score, weight variation, and spleen weight. In our novel, DSS-induced colitis animal model, the lack of an oxidative burst ROS was sufficient to develop adenocarcinoma, and display altered blood plasma metabolic and lipid profiles. Thus, oxidative burst seems to be necessary to prevent evolution toward cancer and may confer a protective role in a ROS-mediated self-control mechanism.
2019-05-22 | MTBLS593 | MetaboLights
Project description:We use single-cell RNA sequencing to analyze cell composition and DEGs of CD45+ cells from spleen, BM, blood, and colon of WT and Wnt5 DKO mice under DSS treatment
2024-03-31 | GSE255409 | GEO
Project description:intestinal mesenchymal stromal cell subset specific accessible elements were analyzed using ATAC-seq Bulk RNA-seq Purpose: The goals of this study are to compare WT and Map3k2 deficient mice colon tissue transcriptome upon Naive and DSS treatment for 1 day Bulk RNA-seq Methods: Colon Tissue mRNA profiles of Naive or 2% DSS treated 16-week-old wild-type (WT) and MEKK2 knockout (Map3k2-/-) mice were generated by deep sequencing, in triplicate, using Illumina NextSeq 500. The sequence reads that passed quality filters were analyzed at the gene level with : Bowtie2 followed by HTSeq-Count and Normalized by DESeq2 Bulk RNA-seq Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the mouse genome (build mm10) and identified 13,284 transcripts in the colon tissues of WT and Map3k2-/- mice. Single-cell RNA-seq Purpose: The goals of this study are to characterize murine colon mesenchymal stromal cell heterogeneity upon DSS treatment for 3 days Single-cell RNA-seq Methods: Mesenchymal Stromal Cell Single Cell Suspension Dissociated from 2% DSS treated 12-week-old wild-type (WT) mice has undergone 10x genomics single cell RNA sequencing using Illumina NextSeq 500. Single-cell RNA-seq Results: Using CellRanger and Seurat we identified 11,284 cells after quality control and filtering
2020-08-15 | GSE156245 | GEO