GEO accession GSE231506 is currently private and is scheduled to be released on Oct 01, 2025.
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ABSTRACT:
PROVIDER: PRJNA966172 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the effect of Vista, a novel immune checkpoint, on intestinal damage of DSS(dextran sulfate sodium)-induced colitis mice.
2025-10-01 | GSE231506 | 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:The role of Trim58 in acute inflammation is so far unclear. The aim of this study was to determine the effects of Trim58 deficiency on acute DSS-colitis in mice. We used microarrays to assess gene expression profiles in middle colons of Trim58-/- vs. Trim58+/+ mice after inflammatory stress-mediated mucosal damage during the regeneration phase.
2019-08-08 | GSE127182 | GEO
Project description:TFEB in IEC has a protective role in DSS colitis. The goal is to examine what genes/pathways are TFEB target during DSS colitis
2018-02-22 | GSE98266 | GEO
Project description:Background: MicroRNAs (miRNAs) acting as negative regulators of gene expression are differentially expressed in intestinal tissues of patients with inflammatory bowel disease (IBD). Assessing the functional role of miRNAs in murine models of colitis facilitates elucidating the role of specific miRNAs in human IBD. The aim of this study was to determine the miRNA signature of murine models of colitis and to assess the influence of miR-21 on intestinal inflammation. Methods: miRNAs expression was accessed by microarray for acute and chronic murine model of colitis induced by DSS or TNBS. miR-21-deficient mouse and littermates controls were assessed in the standard DSS, TNBS and CD4+ T cell transfer models of colitis. RNAs of mouse colon and CD4+CD45RBHigh cells were analyzed by miRNA and mRNA microarray, and quantitative RT-PCR. Th1 polarization was accessed by flow-cytometry and ELISA. Results: Alterations of in miRNAs expression were identified for acute and chronic DSS colitis and TNBS colitis, receptively. The Expression of miRs-21, -142-3p and -223 was were distinct between DSS and TNBS models while overlap of numerous miRNAs was seen. Importantly, miRs-19b, -192 and -215, that are decreased in IBD, were significantly decreased in all 4 models of colitis. miR-21, which is increased in IBD, was increased in TNBS colitis but not the DSS colitis models. Further assessment of the miR-21-deficient 1-/- mice revealed that the deletion of miR-21 results in the exacerbation of both the TNBS and T cell-transfer models of colitis. Conclusions: miRNAs are differentially expressed in both human IBD and murine colitis, with overlap of several IBD-associated miRNAs. The demonstration that miR-21 deletion exacerbated CD4+ T cell-mediated models of colitis provides further evidence that miRNAs play significant roles in the pathogenesis of IBD. miRNAs expression was accesed for acute and chronic murine model of colitis induced by DSS or TNBS.Total of 20 samples with duplicates were analyed in this study.
2014-07-23 | E-GEOD-59649 | biostudies-arrayexpress
Project description:Analysis of the effect of A. caninum ES proteins on a DSS-induced mouse model of colitis
2016-12-05 | PXD004369 | Pride
Project description:Abstract. Ulcerative colitis (UC) is an intestinal disease characterized by chronic recurrent inflammation, but the underlying mechanism remains undefined and requires in-depth exploration. The aim of the present study was to investigate the biological effects of a small molecular compound M1002 of oxygen-sensing signaling pathway on dextran sulfate sodium (DSS)-induced intestinal inflammation colitis mouse models. It was found that the protective effects of M1002 on DSS-induced colitis. To determine how M1002 exerted its protective effect in DSS-induced colitis, we compared the global gene expression profiles in the gut between DSS control and M1002 treatment colitis mouse groups by RNA-Seq. The results demonstrated that HIF-1 signaling pathway-related genes were significantly upregulated in the gut of M1002 treatment colitis mice, whereas the Inflammatory bowel disease signaling pathway, the TNF signaling pathway, and Cytokines and inflammatory response signaling pathway related genes were significantly downregulated in the M1002 treatment group. 16S rRNA gene sequencing demonstrated remarkable variations in the composition of gut microbiota between DSS control and M1002 treatment colitis mice. Compared with DSS control colitis mice, the relative abundance of Eubacterium_nodatum and Halomonas in the gut microbiota was significantly increased at genus level in the gut of M1002 treatment colitis mice. Based on these findings, we tend to conclude that M1002 might alleviate DSS-induced gut injury in mice by regulation of HIF-1 signaling and up-regulating Eubacterium_nodatum and Halomonas.
2025-07-01 | GSE271173 | GEO
Project description:Ulcerative colitis (UC), a subtype of inflammatory bowel disease (IBD), is characterized by chronic and relapsing mucosal inflammation initiating in the rectum and extending upward through part or the entire colon in a continuous fashion. Currently, 5-aminosalicylic acid agents, corticosteroids, immunomodulators, and surgery are the main treatments for UC, which are limited in clinical practice due to common nonadherence, serious adverse effects and heavy financial burden. Atractylodes macrocephala Koidz. (Baizhu) has been used for improving gastrointestinal function and treating digestive disorders for thousands of years, and is currently one of the most frequently used traditional Chinese medicines for the treatment of UC. The purpose of this study was to evaluate the effect and underlying mechanism of polysaccharide from Atractylodes macrocephala Koidz. (PAMK) on UC based on a mouse model of dextran sodium sulfate (DSS)-induced colitis. To investigate the mechanism of therapeutic effect of PAMK on colitis, we performed the microarray analysis of colonic tissues in Control, DSS and DSS+PAMK groups. The results indicated that the beneficial effect of PAMK on DSS-induced colitis may rely on the regulation of the immune response.
2022-10-14 | GSE211359 | GEO
Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days
2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress
Project description:RNA-seq from colon tissues of mice treated with 3%DSS at various stages of colitis development and resolution.
2021-02-11 | E-MTAB-9850 | biostudies-arrayexpress