Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA210513 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression. The DSS-treated colons derived from WT (n=3) and STAP-2 KO (n=3) mice were examined. Each strain was run in biological duplicate.
2014-04-17 | E-GEOD-48543 | biostudies-arrayexpress
Project description:To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression.
2014-04-17 | GSE48543 | GEO
Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.
2025-09-18 | PXD063633 | Pride
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
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 analysis of sorted colon macrophages of Rictor fl/fl LysM+/+ and Rictor fl/fl LysM+/cre mice Dysregulations of immune and metabolic processes can lead to chronic inflammation, which is one of the driving forces for the development of cancer. Macrophages are regulators of these processes and therefore have a fundamental role for the initiation of cancer. Here we find that deletion of Rictor in myeloid cells increases tumor number and size in the colitis-associated colorectal cancer model and leads to a stronger inflammatory response in the underlying acute DSS-colitis model. OPN is shown to be upregulated in the serum of myeloid-specific Rictor-KO mice during the DSS-colitis and the more severe phenotype, characterized by decreased survival, increased weight loss, shorter colons and enhanced infiltration of immune cells into the colon, can be reverted by the neutralization of OPN in these mice. Microarray analysis reveals a change in inflammatory and metabolic gene signatures of Rictor-KO colon macrophages that is also seen in the Rictor-KO BMDM in vitro. Therefore, our data show that myeloid Rictor controls macrophage polarization and the cellular energy metabolism, thereby suppressing colitis and colitis-associated colorectal cancer.
2019-11-12 | GSE96525 | GEO
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.
2010-10-13 | GSE22307 | GEO
Project description:Expression data from colon epithelium of STAT3IEC-KO in acute DSS colitis
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Project description:To investigate the detailed molecular mechanisms for the regulatory role of Nik in colitis, microarray gene expression analysis was performed on colon tissue RNA isolated from 3-month-old untreated control and DSS treated Nik+/+ and NikΔIE mice.
2019-01-08 | GSE86194 | GEO
Project description:Dextran Sulfate Sodium (DSS) is widely used to model colitis due to its ability to disrupt the colonic epithelial barrier and trigger inflammation. While DSS is a valuable tool for studying colitis-related diseases, its impact on mitochondrial bioenergetics and the proteomic landscape of colonic tissue remains poorly understood. To address this gap, we administered 3% DSS in drinking water to C57BL/6J mice and analyzed resected colonic tissue from treated and control mice. Longitudinally opened colon segments were cleaned and subjected to high-resolution respirometry and mass spectrometry-based proteomic profiling. DSS treatment led to a global lowering of mitochondrial respiration, with the most pronounced impairments observed in complex I-supported respiration. Proteomic analysis revealed that these functional deficits occurred largely independently of changes in the mitochondrial proteome, except for an upregulation of NIPSNAP1, a mitophagy-related protein. However, lentiviral knockdown of NIPSNAP1 in HCT116 cells did not rescue the observed bioenergetic defects, suggesting it is not the primary driver. Collectively, our findings show that DSS impairs mitochondrial respiration in the colon—most notably at complex I—without major alterations to the mitochondrial proteome. Given the role of mitochondrial dysfunction in various diseases, these effects should be carefully considered when using DSS-based models to study colitis pathophysiology.
2025-09-26 | PXD065807 | JPOST Repository