Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ER-464195-01 regulates the expression of inflammation-related genes in DSS-treated mice

ABSTRACT: We identified a small molecule, orally active ER-464195-01, inhibits the calreticulin binding to alpha integrins, and clearly suppresses the adherence ability of leukocytes. Our transcriptome analysis with the colon of dextran sodium sulfate (DSS)-treated mice reveals that the increased expression of pro-inflammatory genes was down-regulated by ER-464195-01. Purpose: To gain insight into the molecular mechanisms underlying the prevention of DSS-induced colitis conferred by treatment of ER-464195-01, we performed a comprehensive analysis of ER-464195-01-mediated gene expression changes in DSS-induced colitis using RNA sequencing (RNA-Seq). Methods: Male Balb/c mice (7 weeks) were allowed free access to distilled water (Otsuka Pharmaceutical) containing 2% DSS (molecular weight: 36,000–50,000; ICN Biomedicals) for 6 days to induce colitis. ER-464195-01 (10 mg/kg) or vehicle was orally administered once per day for 6 days. Results: To investigate differentially expressed genes (false discovery rate (FDR) p<0.05, fold change >2) among three groups, we performed pairwise comparisons of RNA-Seq data using the CLC Genomics Workbench software. In comparison with the control, 5,570 (3,483 up- and 2,087 down-regulated) unique genes were significantly changed in the DSS-induced colitis group. Meanwhile, the data set of DSS-induced colitis with ER-464195-01 groups revealed significant changes in 1,808 (837 up- and 971 down-regulated) genes as compared with DSS alone. Notably, of 3,483 genes up-regulated by the DSS treatment, 894 transcripts of which were overlapped with 971 genes down-regulated genes by ER-464195-01.

ORGANISM(S): Mus musculus

PROVIDER: GSE98407 | GEO | 2018/04/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of ER-464195-01 on the gene expression in the intestine of mice.

Project description:Our previous study identified a small molecule, orally active ER-464195-01, inhibits the calreticulin binding to alpha integrins, and clearly suppresses the adherence ability of leukocytes. Our transcriptome analysis with the colon of dextran sodium sulfate (DSS)-treated mice reveals that the increased expression of pro-inflammatory genes was down-regulated by ER-464195-01. Male Balb/c mice (7 weeks) were allowed free access to distilled water (Otsuka Pharmaceutical). ER-464195-01 (10 mg/kg) or vehicle was orally administered once per day for 6 days.

2018-04-11 | GSE109728 | GEO

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

Gene expression profile of ATF6a and ATF6b knockout mice with dextran sulfate sodium (DSS)-induced colitis

Project description:To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR. Colitis was induced with 3% DSS, 36,000-50,000 M.W. (MP Biomedicals,) in the drinking water for 3 days. Genes responsible for DSS treatment in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.

2015-02-08 | E-GEOD-35651 | biostudies-arrayexpress

RNA-Seq from the colon tissues of DSS treated mice receiving either EP4-D, a selective E-type prostanoid receptor 4 agonist or vehicle

Project description:The experiment was designed to identify transcriptomic changes induced by selective EP4 agonism during experimental colitis. The mice received 1mg/ kg of the selective EP4 agonist, EP4-D or sterile phosphate buffered saline as vehicle control orally once per day concomitant with 3% DSS in drinking water. The DSS treatment was stopped on day 5 and mice were provided access to autoclaved drinking water for 3 additional days along with agonist and vehicle treatments once daily as described above. At the end of the treatment period, colon tissues from the mice were harvested, RNA isolated, and sequenced to identify transcriptional changes.

2021-02-01 | E-MTAB-9820 | biostudies-arrayexpress

Project description:DSS-induced colitis

| PRJNA693887 | ENA

Apple peel polyphenolic content as a key player for the prevention and treatment of experimental inflammatory bowel disease.

Project description:Colonic gene expression profiles of mice with DSS-induced colitis treated with apple peel polyphenolic extract Four-condition experiment: control, DSS-induced colitis, and mice treated with DAPP (two different doses (200 and 400 mg/kg/day) before or during induction and development of DSS-induced colitis.

2016-12-06 | GSE71920 | GEO

Immunoregulatory actions of T cell PPAR g at the colonic mucosa

Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. METHODS: Wild-type (WT) or PPAR g flfl; CD4 Cre+ (CD4cre) mice in a C57BL/6 background were challenged with 2.5% DSS in their drinking water for 0, 2, or 7 days. Mice were scored on disease severity both clinically and histopathologically. Flow cytometry was used to assess lymphocyte and macrophage populations in the blood, spleen, and mesenteric lymph nodes (MLN). Global gene expression in colonic mucosa was profiled using Affymetrix microarrays. RESULTS: Both disease severity and inflammation-related body weight loss were accelerated by the deficiency of PPAR g in T cells. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than wt mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively. Transcriptomic profiling revealed around 3000 genes being transcriptionally altered as a result of DSS challenge in CD4cre mice. These included up-regulated adhesion molecules on day 7 and proinflammatory cytokines interleukin-6 (IL-6) and IL-1b, and suppressor of cytokine signaling 3 (SOCS-3) mRNA expression. CONCLUSIONS: These findings suggest that T cell PPAR g down-regulates inflammation during DSS colitis by inhibiting colonic expression of inflammatory mediators and increasing MLN Treg. Colonic mucosa from wt and CD4cre mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis

2010-07-08 | E-GEOD-20523 | 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

H3K27me3 analysis in mouse colonic epithelial cells

Project description:H3K27me3 statuses were analyzed in normal mouse colonic epithelial cells and in those exposed to DSS-induced colitis, and aberrant changes of H3K27me3 by DSS-induced colitis were identified.

2015-10-15 | GSE74007 | GEO

RNA Sequencing Analysis of macrophages from Wild Type and Gsdmd-/- colitis mice

Project description:We identified that GSDMD protected against DDS-induced colitis, and GSDMD deficiency in macrophages promoted the development of DSS-induced colitis.The purpose of this experiment was to identify how GSDMD protected against DSS-induced colitis.

2020-07-06 | GSE137827 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data