Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-42768
PROVIDER: PRJNA183090 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease. We used whole gene expression arrays to study differences in colonic gene expression levels between acute and more chronic DSS colitis, Acute and chronic relapsing colonic inflammation was induced in C57BL6 female mice using several cycles of exposure to DSS in drinking water, followed by recovery phases. Total RNA, extracted from snap frozen colon from five mice per condition was used to analyze mRNA expression via Affymetrix Mouse Gene 1.0 ST arrays.
2013-09-03 | E-GEOD-42768 | biostudies-arrayexpress
Project description:The lack of suitable animal models reflecting chronically relapsing inflammation and tissue remodeling have hindered fibrosis research in inflammatory bowel diseases (IBD). This study investigated changes in connective tissue in a chronic murine model using different cycles of dextran sodium sulphate (DSS) to mimic the relapsing nature of the disease. We used whole gene expression arrays to study differences in colonic gene expression levels between acute and more chronic DSS colitis,
2013-09-03 | GSE42768 | GEO
Project description:Increased levels of tissue inhibitor of metalloproteinase-1 (TIMP-1) have been detected in fibrotic strictures in Crohnâs disease. In a murine model of chronic inflammation, fibrosis was associated with an increase in TIMP-1 and inhibition of matrix metalloproteinase (MMP)-mediated degradation. We investigated the effect of TIMP-1 deficiency on the colonic gene expression in acute and chronic murine models of colitis, using whole genome gene expression arrays. Colitis was induced via oral administration of dextran sodium sulphate (DSS) to B6.129S4-Timp1tm1Pds/J knock-out (KO) and C57BL/6J wild-type (WT) mice. Total RNA extracted from snap frozen colon was used to analyze mRNA expression via Affymetrix Mouse Gene 1.0 ST Arrays
2016-07-22 | E-GEOD-73424 | biostudies-arrayexpress
Project description:Protracted inflammatory responses are signatures common to many gastrointestinal disorders. Severe and chronic disorders often bring about extensive tissue damage, in turn leading to hypercytokinemia. Here, we show that stimuli like dextran sulphate sodium salt (DSS) and stearic acid (SA) cause acute colonic inflammation, and ANGPTL4 is an important regulator in mediating the extent of colonic inflammation. Using comparative microarray gene expression analysis, we seek to identify genes whose expression are altered during inflammation between ANGPTL4+/+ and ANGPTL4-/- mice.
2017-03-28 | GSE78500 | GEO
Project description:Primary cilia (PC) are important signaling hubs in cells and we explored their role in colorectal cancer (CRC) and colitis. In the colon we found PC to be mostly present on different subtypes of fibroblasts and exposure of mice to either chemically induced colitis-associated colon carcinogenesis (CAC) or dextran sodium sulfate (DSS)-induced acute colitis decreased PC numbers. We employed conditional knock-out strains for the PC essential genes, Kif3A and Ift88, to generate mice with reduced numbers of PC on colonic fibroblasts. These mice showed an increased susceptibility in the CAC model as well as in DSS-induced colitis. Secretome and immunohistochemical analyses of DSS-treated mice displayed an elevated production of the pro-inflammatory cytokine IL-6 in PC-deficient colons. An inflammatory environment diminished PC presence in primary fibroblast cultures. This was triggered by IL-6 as identified by RNAseq analysis together with blocking experiments, suggesting an activation loop between IL-6 production and PC loss. Notably, an analysis of PC presence on biopsies of patients with ulcerative colitis as well as CRC patients revealed decreased numbers of PC on colonic fibroblasts in pathological versus surrounding normal tissue. Taken together, we provide evidence that a decrease in colonic PC numbers promotes colitis and CRC.
2022-11-29 | PXD033440 | Pride
Project description:We characterized the transcriptional landscape of acute and chronic models of dextran sodium sulfate (DSS) and adoptive transfer (AT) colitis murine models to derive novel temporal gene expression and splicing signatures in blood and colonic tissue in order to capture dynamics of colitis remission and relapse. We show that colitis induces robust expression of minor isoforms and using machine learning, demonstrate that specific temporal gene expression and splicing signatures are highly predictive of tissue histopathology spanning blood and colonic tissue as well as various experimental sites and protocols. Finally, we identified sub networks of patient-derived causal networks that were enriched in these temporal signatures to distinguish acute and chronic disease components within the broader molecular landscape of IBD.
2022-12-31 | GSE214600 | GEO
Project description:The goal of this project is to investigate the role of glucocorticoids and their receptor, glucocorticoid receptor (GR), in intestinal stress response and tissue homeostasis. Using a mouse model with specific deletion of GR in intestinal epithelium (GR iKO mice), we recently discovered that intestinal epithelial GR deficiency deteriorates acute colitis while reducing chronic inflammation-associated colon cancer formation in mice. To understand the molecular mechanisms underlying these phenotypes, we examined colonic transcriptomes of Flox control and GR iKO mice treated with or without dextran sulfate sodium (DSS) for 7 days by microarray analysis.
2021-11-15 | GSE146048 | GEO
Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Keywords: Time course and differentially expressed genes analysis
2008-11-01 | GSE9281 | GEO
Project description:Background and Aims. Dendritic cells (DCs) play a pivotal role in maintaining immunological homeostasis by orchestrating innate and adaptive immune responses via migration to inflamed sites and the lymph nodes (LNs). Plasmacytoid DCs (pDCs) have been reported to accumulate in the colon of inflammatory bowel disease (IBD) patients and dextran sulfate sodium (DSS)-induced colitis mice. However, the role of pDCs in the progression of colonic inflammation remains unclear. Methods. 80 compounds in natural medicines were searched for inhibitors of pDC migration using bone marrow-derived pDCs (BMpDCs) and conventional DCs (BMcDCs). BALB/c mice were given 3% DSS in the drinking water for 7 days to induce acute colitis. Compounds, which specifically inhibited pDC migration, were administrated into DSS-induced colitis mice. Results. Astragaloside IV (As-IV) and oxymatrine (Oxy) suppressed BMpDC migration but not BMcDC migration. In DSS-induced colitis mice, the number of pDCs was markedly increased in the colonic lamina propria (LP), and the expression of CCL21 was obviously observed in colonic isolated lymphoid follicles (ILFs). As-IV and Oxy reduced symptoms of colitis and the accumulation of pDCs in colonic ILFs but not in the colonic LP. Moreover, in a BMpDC adoptive transfer model, BMpDC migration to colonic ILFs was significantly decreased by treatment with As-IV or Oxy. Conclusion. pDCs accumulated in the colon of DSS-induced colitis mice, and As-IV and Oxy ameliorated DSS-induced colitis by suppressing pDC migration to colonic ILFs. Accordingly, the selective inhibition of pDC migration may be a potential therapeutic approach for treating colonic inflammatory diseases.
2021-07-06 | GSE167388 | GEO
Project description:Background & Aims: Dextran sulphate sodium (DSS) induced colitis in rats is one of the most widely used models of inflammatory bowel disease. Animal models can provide new insights into the pathogenesis of intestinal inflammation, which is still unknown. We have performed a genomic analysis of the DSS rat colitis including an acute and a recovery phase. Methods: Expression profile of 6 control rats were compared with colitic rats at day 1 every other day until day 23 after DSS treatment using the GeneChip Rat Genome 230 2.0 Array (Affymetrix). Functional and pathways analysis were made with the differentially expressed genes. Experiment Overall Design: Experimental design: DSS was administered to animals in drinking water as follows:5%DSS from day 1 to 7, 3%DSS from day 8 to 15, 0% DSS from day 16 to 23. Samples were recovered at days 1, 3, 5, 7 (5%DSS), 9, 11, 13, 15 (2%DSS), 17, 19, 21 and 23 (0%DSS). According to inflammatory markers (Myeloperoxidase activity activity, body weight loss, colonic weigth/length ratio), three replicates at each time point were selected for genomic analysis and 6 control healthy rats (42 arrays). Experiment Overall Design: RNA was extracted from homogenized full-thickness colonic tissues in Trizol® reagent (Invitrogen) and purified with RNeasy affinity columns (Qiagen), according to manufacturer´s protocol. The microarray analysis was performed by Progenika Biopharma (Bilbao, Spain) on GeneChip® Rat Genome 230 2.0 Array (Affymetrix). All sample labeling (biotin), hybridization, staining and scanning procedures were carried out using Affimetrix, standard protocols (www.affymetrix.com). Normalization was carried out using Bioconductor sofware (affyPLM package).
2008-11-13 | E-GEOD-9281 | biostudies-arrayexpress