Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1131294 | ENA |
REPOSITORIES: ENA
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Project description:To clarify the pathological significance of CGRP in ulcerative colitis, we generated knockout mice for CGRPα and CGRPβ and analyzed colon proteome data from DDS drinking water ulcerative colitis model mice. In addition, to confirm changes in the colon over time, the colon of wild-type mice after DDS drinking was harvested over time and used for proteome data.
2024-09-23 | PXD055368 | JPOST Repository
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the effects of macrophage-specific E4BP4 overexpression under c-fms gene promoter on colon macrophages during the recovery phase of Dextran Sodium Sulfate (DSS)-induced colitis. Methods: We generated transgenic mice (TG) with macrophage-specific E4BP4 overexpression. Colon macrophages were isolated at Zeitgeber Time (ZT) 0 from TG mice and WT littermates and total RNA was extracted. Colon macrophage RNA profiles were generated by deep sequencing for two groups with three mouse samples each. Results: There were significant differences between TG and WT mice. Conclusions: Colon macrophages from the E4BP4 transgenic mice during the recovery phase of DSS-induced colitis might be altered at the transcription level.
2024-03-31 | GSE183075 | GEO
Project description:To obtain insight into the complex traits underlying the local pathophysiological response to the repeated colitis inductions with TNBS, whole genome gene expression was performed on RNA isolated from the distal colon tissue of 5 mice/timepoint Total RNA obtained from isolated from the distal colon of TNBS colitis mice (isolated on day 9, 14, 16, 21, 23, and 28) was compared to those healthy control mice
2013-07-08 | E-GEOD-35609 | biostudies-arrayexpress
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
Project description:Single-cell RNA-seq has colon epithelial cell analysis of colonoids transplanted colon tissue. The goals of this study are to colonoid engrafted tissue transcriptome profiling (RNA-seq) to define theraputic effect in radiation colitis mice.
2020-07-09 | GSE154014 | GEO
Project description:DSS-induced colitis mice were treated with PBS, A. muciniphila secreting extracellular vesicles (SEV) via gavage every day. mice colon tissues from each of the indicated group (Ctrl, Colitis and SEV) in (b) were collected. Mice colon tissues were submitted for scRNA-seq.
2023-01-01 | GSE211578 | GEO
Project description:To understand how specifically intestinal ERβ impacts the transcriptome during colitis and tumor develpment, sequencing was perfromed on colon epithelium from AOM/DSS or vehicle treated mice, and tumors from treated mice.
2025-07-21 | GSE271135 | GEO
Project description:In the DSS-induced colitis model, the epithelial damage and resulting inflammation is restricted to the colon, with a potential influence on the microbial composition in the adjacent cecum. Several studies have reported changes of the gut microbiota in the DSS-induced colitis model and other mouse models of IBD. Furthermore, metaproteomics analysis of the gut microbiome in a mouse model of Crohn’s disease demonstrated that disease severity and location are microbiota-dependent, with clear evidence for the causal role of bacterial dysbiosis in the development of chronic ileal inflammation. We have developed a refined model of chronic DSS-induced colitis that reflects typical symptoms of human IBD without a risky body weight loss usually observed in DSS models [Hoffmann et al., submitted]. In this study, we used metaproteomics to characterize the disease-related changes in bacterial protein abundance and function in the refined model of DSS-induced colitis. To assess the structural and functional changes, we applied 16S rRNA gene sequencing and metaproteomics analysis of the intestinal microbiota in three different entities of the intestinal environment, i.e. colon mucus, colon content and cecum content.
2020-03-17 | PXD007220 | Pride
Project description:Purpose: The goals of this study are to confirm the hypothesis that E4BP4 regulates colon specific anti-inflammatory macrophage. Methods: We generated transgenic mice (TG) with macrophage-specific E4BP4 overexpression. CD45+ cells in colon lamina propria were isolated at Zeitgeber Time (ZT) 0 from TG mice and WT littermates during the recovery period of dextran sulfate sodium (DSS)-induced colitis, and total RNA was extracted. CD45+ cells in colon lamina propria RNA profiles were generated by deep sequencing for two groups with one mouse sample each. Results: There were significant differences between TG and WT mice. Conclusions: E4BP4 increased the number of M2 macrophage population and upregulated anti-inflammatory genes.
2024-03-31 | GSE183529 | GEO