Project description:Ribo-zero RNAseq experiments were carried out with mouse distal colon DSS Colitis model of genetically engineered mice. For each mouse line for: Gpsm3 (3% DSS), Aif1 (3% DSS), Nckap1l (Hem1), Dock2 (3% DSS), Dok3 (3.5% DSS) DSS treatment for five days followed by water for 5 days, (7 days for Nckap1l). Tissue was collected at Day 10 (Day 12 for Nckap1l (HEM1)).
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.
Project description:B cells expand during the recovery after DSS-induced colonic inflammation. To investigate if a specific subtype is expanding and to analyse the transcriptional profile of these cells a transcriptional analysis on single cell level was carried out. In detail, B cells were isolated from the colon of mice on day 0 (no treatment) or day 14 (recovery) after 7 days of DSS treatment by flow cytometric sorting and analyzed by 10X sequencing.
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
Project description:Expression profile of colon mucosa of F344 rats treated with 5% DSS during five days vs colon mucosa of F344 rats pre-treated for 20 days with resveratrol 1mg/kg/day and during the five days of 5% DSS administration Keywords: Inflammation experiment Two conditions experiment, colon mucosa of F344 rats treated 5% DSS for 5d vs colon mucosa of F344 rats pretreated with 1mg/kg/day resv + 5% DSS for 5d. 8 Biological samples for each group
Project description:The identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase paralleling the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b-/- mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. Atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohn’s disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b-/- mice. Taken together, these results provide additional evidence on the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that Atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency Seven samples were collected in total: three from wild-type mice (1 from the ileum and the colon of control mice, and 1 from the colon of a DSS-treated mouse) and four from Atg4b knock-out mice (1 from the ileum and the colon of control mice, and 2 from the colon of DSS-treated mice).
Project description:intestinal mesenchymal stromal cell subset specific accessible elements were analyzed using ATAC-seq Bulk RNA-seq Purpose: The goals of this study are to compare WT and Map3k2 deficient mice colon tissue transcriptome upon Naive and DSS treatment for 1 day Bulk RNA-seq Methods: Colon Tissue mRNA profiles of Naive or 2% DSS treated 16-week-old wild-type (WT) and MEKK2 knockout (Map3k2-/-) mice were generated by deep sequencing, in triplicate, using Illumina NextSeq 500. The sequence reads that passed quality filters were analyzed at the gene level with : Bowtie2 followed by HTSeq-Count and Normalized by DESeq2 Bulk RNA-seq Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the mouse genome (build mm10) and identified 13,284 transcripts in the colon tissues of WT and Map3k2-/- mice. Single-cell RNA-seq Purpose: The goals of this study are to characterize murine colon mesenchymal stromal cell heterogeneity upon DSS treatment for 3 days Single-cell RNA-seq Methods: Mesenchymal Stromal Cell Single Cell Suspension Dissociated from 2% DSS treated 12-week-old wild-type (WT) mice has undergone 10x genomics single cell RNA sequencing using Illumina NextSeq 500. Single-cell RNA-seq Results: Using CellRanger and Seurat we identified 11,284 cells after quality control and filtering
Project description:The purpose of this study was to determine which genes are differentially regulated by the Ras-related small GTPase RBJ after induction by AOM/DSS treatment in the colon of C57BL/6 mice compared to RBJ+/+ mice. The results demonstrate decreased induction of cell proliferation-associated genes in RBJ-/- mice than in RBJ+/+ mice on day 80 after AOM/DSS treatment. The majority of differentially expressed genes are regulated by MEK/ERK signaling pathway. Thus RBJ may be involved in the regulation of tumor progression and tumorigenesis.
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.