E-GEOD-22307
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA127385
PROVIDER: E-GEOD-22307 | ExpressionAtlas | 2015-01-06
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:We showed different function of monocyte derived cells in the lamina propria of the colon under steady state and inflammatory conditions. We used microarrays to detail the global programme of gene expression and identified distinct clusters of regulated genes during this process. Different subsets of mononuclear phagocytes were sorted from the colonic lamina propria as well as the spleen. Sorting was done in C57BL/6 mice in steady state and under inflammatory conditions (Dextran Sodium Sulphate induced colitis model)
2012-11-08 | E-GEOD-42101 | biostudies-arrayexpress
Project description:The effect of Cardamonin was checked on Dextran sulfate sodium and Azoxymethane (AOM) induced colon cancer in C57Bl/6 mice. C57Bl/6 were given a single AOM (10mg/kg B.wt) intraperitonielly at day 0 and three bouts of 5% DSS at days 5-10, 25-30, 45-50. At day 140, the mice were sacrificed and colon was monitored for tumors. Cardamonin treatment (10mg/Kg B.wt, p.o) was started simulatenously for one group. For the second group it was started after 16 of first AOM injection. The study was terminated at 140 day. The RNA was ioslated uisng mirVANA kit from each samples followed miRNA analysis uisng affymetrix gene chip miRNA array 4.0
2021-04-07 | GSE121608 | GEO
Project description:The aim of the project is to determine the impact of NUAK1 depletion on the transcriptome of in situ colon tumours. Tumours were initiated in Villin-CRE-ER;APC-floxed;DI-shNUAK1 mice, followed by treatment for 1 week with dextran sodium sulphate. 68 days after tumour initiation, NUAK1 shRNAs were induced by doxycycline administration (via gavage), or left un-induced. 6 tumours were harvested from NUAK1 shRNA expressing mice and 6 from controls. RNA was isolated using Qiagen RNEasy and analyzed by Illumina paired-end RNA-SEQ
2018-02-19 | E-MTAB-6265 | biostudies-arrayexpress
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
Project description:The current study was designed to clarify signalling pathways and assess possible beneficial effect of new probiotic mixture in DSS (dextran sulphate sodium) – induced colitis mouse model. Manipulation of intestinal microbiota with probiotics represents a promising alternative or adjunct therapy in gastrointestinal disorders and inflammation. RNA extracted from the middle part of colon tissue from ~11 weeks female C57BL/6JOlaHsd mouse strain was used for examination of the global gene expression using Affymetrix GeneChip Mouse Gene 2.0 ST microarrays.
2018-03-23 | GSE89851 | GEO
Project description:Folic acid supplementation (8 mg/kg diet) promotes colon tumor formation in mice with established colitis induced by carcinogen azoxymethane (AOM) and dextran sulfate sodium sulfate (DSS). This induction of colon tumors was associated with hypomethylation of DNA cased by folic acid supplementation.
2023-05-31 | GSE168525 | GEO
Project description:Folic acid supplementation (8 mg/kg diet) promotes colon tumor formation in mice with established colitis induced by carcinogen azoxymethane (AOM) and dextran sulfate sodium sulfate (DSS). This induction of colon tumors was associated with hypomethylation of DNA cased by folic acid supplementation.
2023-09-07 | GSE168975 | GEO
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 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.
2014-01-14 | E-GEOD-54035 | biostudies-arrayexpress
Project description:Colorectal cancer (CRC) was induced in Foxp3/eGFP reporter mice by the azoxymethane/dextran sulphate sodium salt (AOM/DSS) protocol. Mice were injected i.p. with the procarcinogen AOM (12.5 mg/kg of body weight). After 1 week, mice received drinking water supplemented with 2.5% DSS for 5 to 7 days, followed by 2 weeks of regular water. The DSS administration was repeated twice with 2% DSS. Mice were sacrificed at week 11 and lamina propia lymphocytes (LPLs) from the colon were isolated. CD4+FOXP3+ (eGFP+) ST2+ or ST2- Tregs were separated from colonic LPLs of CRC induced mice using a FACSAria II cell sorter. Microarray analysis was performed to analyze if ST2+ FOXP3+ Tregs from the colon of CRC mice present a distinct transcription pattern compared to ST2- FOXP3+ Tregs. By this, the role of ST2 for Treg function during intestinal tumorigenesis should be characterized.
2019-05-31 | E-MTAB-6842 | biostudies-arrayexpress
Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.
2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress