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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

ABSTRACT: Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine whether genes altered in the normal colonic epithelium or tumor differed between sporadic and inflammation-associated tumor development. 97 day old (ACIxF344)F1-Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions. Normal colonic tissue and tumors were harvested from the distal colon at 97 days of age. A two color, reference design experiment hybridized according to Agilent protocols against a reference pool of RNA made up from colon tissue taken from pooled wild type rats which was labeled with Cy5.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Amy Irving

PROVIDER: E-GEOD-54035 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The concentrations of EGFR, LRG1, ITIH4, and F5 in serum correlate with the number of colonic adenomas in ApcPirc/+ rats.

Ivancic Melanie M MM Irving Amy A AA Jonakin Kelli G KG Dove William F WF Sussman Michael R MR

Cancer prevention research (Philadelphia, Pa.) 20140908 11

The development of noninvasive methods for early detection of colon cancer is critical for the successful management of this disease. Using a targeted quantitative proteomics technique, we assessed the ability of 12 serum proteins to detect the presence of colonic polyps in the Apc(Pirc) (/+) rat model of familial colon cancer. Serum protein candidates were selected from gene transcripts upregulated in colonic tumors of Apc(Pirc) (/+) rats and from a prior study of serum proteins differentially ...[more]

PMID: 25200834

Similar Datasets

Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

Project description:Dextran sodium sulfate (DSS) causes inflammation in the gut similar to ulcerative colitis in humans. Patients with ulcerative colitis have increased risk of developing colon cancer. We sought to determine which genes are altered in the normal colonic epithelium, and which changes depend on the Pirc mutation. 97 day old (ACIxF344)F1 wild type and Pirc male rats either untreated or given 4% DSS in the drinking water from 40-47 and 54-61 days of age, housed in 12 hour light:12 dark, ad lib feeding. Normal colonic tissue was collected from the distal colon at 97 days of age.

2014-01-14 | E-GEOD-54005 | biostudies-arrayexpress

Loss of colonic primary cilia promotes inflammation and carcinogenesis

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

Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis.

Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.

2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress

Expression data from mouse colon tissue response to DSS induction at day 0, 2, 4 and 6

Project description:Temporal genome profiling of DSS colitis The DSS induced mouse colitis model is often used to emulate Ulcerative Colitis (UC) in order understand pathophysiological mechanism of inflammatory bowel disease (IBD). Given the progressive nature of IBD, colon tissue gene expression changes during the evolution of disease, and knowing the changes in gene expression profiles could indentify potential diagnostic markers or additional therapeutic targets for colitis. Therefore, we performed temporal genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with the development of colitis. Keywords: Expression time course of mouse colon tissue induced by 3% DSS. C57BL/6J mice were given 3% DSS in the drinking water and tissues from individual cohorts were collected at days 0, 2, 4 and 6. Total RNA were extracted from the colon tissue and detected by Affymerix GeneChip Mouse Genome 430 2.0 Array.

2010-10-13 | E-GEOD-22307 | biostudies-arrayexpress

Gene expression profiling of colitis-associated and sporadic colorectal tumors in mice

Project description:To uncover molecular mechanisms specifically involved in the pathogenesis of colitis-associated colon cancer (CAC), we studied tumorigenesis in experimental models of CAC and sporadic CRC that mimic characteristics of human CRC. Using comparative whole genome expression profiling, we observed differential expression of epiregulin (Ereg) in mouse models of colitis-associated, but not sporadic colorectal cancer. Similarly, highly significant upregulation of Ereg expression was found in cohorts of patients with colitis-associated cancer in inflammatory bowel disease but not in sporadic colorectal cancer. Furthermore, tumor-associated fibroblasts were identified as major source of Ereg in colitis-associated neoplasias. Functional studies showed that Ereg-deficient mice, although more prone to colitis, are strongly protected from colitis-associated tumors, and data from serial endoscopic studies revealed that Ereg promotes growth rather than initiation of tumors. 4 samples of individual distal colitis-associated tumors (CAC) from 4 mice, 2 samples of tumor-free distal colon epithelium with a pool of 5 mice per sample (CAC contr), 5 samples of individual Apcmin/+ tumors from the distal colorectum of 5 mice (sporCRC) and 3 samples of tumor-free distal colon epithelium (pool of 4 mice per sample) (sporCRC contr). Colitis-associated tumorigenesis was performed by intraperitoneal injection of Azoxymethane (10mg/kg) (Sigma) into C57BL/6J wildtype mice followed by 3 cycles of Dextran Sodium Sulfate (DSS) in drinking water. Each DSS-cycle was composed of DSS (2.5% (w/v) (MP Biomedicals) in drinking water for 7 days, followed by a recovery phase with regular drinking water for 14 days. Sporadic tumors were from C57BL/6J-ApcMin/+/J mice. All tumors were obtained from the from the lower 6th of the large intestine and they had the same size covering between Â¼ and up to Â½ of the colonic circumferenc as evaluated by mini-endoscopy.

2013-04-01 | E-GEOD-43338 | biostudies-arrayexpress

Composition of the Colonic Mesenchyme and the Nature of its Plasticity in Inflammatory Bowel Disease

Project description:10x Chromium single cell RNA-Seq of colonic mesenchyme cell populations in health and Ulcerative Colitis in human patients and health in DSS-induced colitis in murine colon

2018-09-27 | GSE114374 | GEO

Expression data from untreated and DSS-treated Adamts12 WT and KO mice

Project description:Adamts12-deficient mice undergo more severe colitis than WT mice after induction with DSS. We used microarrays to determine the gene expression differences between Adamts12-deficient and WT mice during ulcerative colitis induced with DSS (dextran sodium sulfate) Fragments of distal colon from DSS-treated (2% DSS during 7 days and 1 day of recovery) and untreated Adamts12-deficient and WT mice were obtained for RNA extraction and hybridiztion with Affymetrix microarrays

2012-09-01 | E-GEOD-40529 | biostudies-arrayexpress

Dextran sodium sulfate treatment of wild type and Pirc rats alters colonic normal tissue gene expression

2014-01-14 | GSE54005 | GEO

Dextran sodium sulfate treatment of Pirc rats alters colonic and tumor gene expression

2014-01-14 | GSE54035 | GEO

Transcriptional reprogramming and resistance to colonic mucosal injury in PARP1-deficient mice

Project description:Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate, and participate to the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator - cytokines, chemokines and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to determine the impact of Parp1 deletion on the innate immune response to mucosal injury. Genome-wide analysis of the colonic transcriptome was performed. Compared to WT, we demonstrated that Parp1-/-were protected from DSS-induced colitis and that this protection was associated with a dramatic transcriptional reprogramming in the colon. WT or Parp1-/- mice were treated with drinking water administered ad libitum without ot with 4% dextran sulfate (DSS) for seven days. Whole colon was collected for RNA extraction and hybridization on Affymetrix microarrays. Thee mice from each genotype/treatment groups were used in the analysis.

2016-01-08 | E-GEOD-76658 | biostudies-arrayexpress

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