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Map3k2-regulated intestinal stromal cells define a distinct intestine stem cell niche for tissue repair

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE156245 | GEO | 2020/08/15

REPOSITORIES: GEO

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Project description:Inflammatory bowel disease is characterized by chronic relapsing idiopathic inflammation of the gastrointestinal tract and persistent inflammation. Studies focusing on the immune-regulatory function of reactive oxygen species (ROS) are still largely missing. In this study, we analyzed an ROS-deficient mouse model leading to colon adenocarcinoma. Colitis was induced with dextran sulfate sodium (DSS) supplied via the drinking water in wild-type (WT) and Ncf1-mutant (Ncf1) B10.Q mice using two different protocols, one mimicking recovery after acute colitis and another simulating chronic colitis. Disease progression was monitored by evaluation of clinical parameters, histopathological analysis, and the blood serum metabolome using 1H nuclear magnetic resonance spectroscopy. At each experimental time point, colons and spleens from some mice were removed for histopathological analysis and internal clinical parameters. Clinical scores for weight variation, stool consistency, colorectal bleeding, colon length, and spleen weight were significantly worse for Ncf1 than for WT mice. Ncf1 mice with only a 7-day exposure to DSS followed by a 14-day resting period developed colonic distal high-grade dysplasia in contrast to the low-grade dysplasia found in the colon of WT mice. After a 21-day resting period, there was still β-catenin-rich inflammatory infiltration in the Ncf1 mice together with high-grade dysplasia and invasive well-differentiated adenocarcinoma, while in the WT mice, high-grade dysplasia was prominent without malignant invasion and only low inflammation. Although exposure to DSS generated less severe histopathological changes in the WT group, the blood serum metabolome revealed an increased fatty acid content with moderate-to-strong correlations to inflammation score, weight variation, colon length, and spleen weight. Ncf1 mice also displayed a similar pattern but with lower coefficients and showed consistently lower glucose and/or higher lactate levels which correlated with inflammation score, weight variation, and spleen weight. In our novel, DSS-induced colitis animal model, the lack of an oxidative burst ROS was sufficient to develop adenocarcinoma, and display altered blood plasma metabolic and lipid profiles. Thus, oxidative burst seems to be necessary to prevent evolution toward cancer and may confer a protective role in a ROS-mediated self-control mechanism.

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Map3k2-regulated intestinal stromal cells define a distinct intestine stem cell niche for tissue repair

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