Project description:To determine how deficiency of Efhd2 in intestinal epithelial cells aggravates DSS-induced colitis in mice, we performed a transcriptional analysis.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to analysis NGS-derived transcriptome profiling (RNA-seq) in DSS induced chronic inflammation, AOM/DSS induced colitis-associated colorectal tumorigenesis and organoids isolation from colitis-associated colorectal tumorigenesis Methods: DSS, AOM/DSS and organoids mRNA profiles of wild-type (WT) and RING Finger 3 (RNF138−/−) mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500. The sequence reads were trimmed for low-quality sequence, then mapped to mm10 whole genome using STAR v2.6.1d Results: Using an optimized data analysis workflow, the padj <0.05 and fold change >2 were refered as differential expression. There are 987, 2649 and 2373 differential genes were found in RNF138-/- compared with Wild Type in DSS, AOM/DSS and organoids, respectively Conclusions: Our study revealed NFκB pathway is the main activation pathway regulated by RNF138 loss
Project description:Total RNA was isolated from 3 colonic tissues of each treatment group using the Qiagen RNeasy kit following the manufacturers' protocol. RNA samples with good quality control (RIN values>8) were sequenced using Hiseq-2500 by Novogene. Ursolic acid (UA), Dextran sulfate sodium (DSS)."Con" group stands for normal group, "DSS" group stands for DSS induced group, "UA_DSS" group stands for UA Preventive DSS induced group, "DSS_UA" group stands for UA Treatment DSS induced group.
Project description:Inflammatory bowel disease (IBD) is a multiple-genes-involved chronic disease and current available targeted drugs for IBD only deliver moderate efficacy. Whether there is a single gene that systematically regulates IBD is not yet known. Here we showed that the expression of miR-146a in colon was elevated in Dextran Sulfate Sodium Salt (DSS)-induced IBD mice and patients with IBD. DSS induced dramatic body weight loss and much more rectal bleeding, shorter colon length and colitis in miR-146a knock-out mice than wild type (WT) mice. The miR-146a mimics alleviated DSS-induced symptoms in both DSS-induced miR-146a-/- and WT mice. Further RNA sequencing illustrated that deficiency of miR-146a de-repressed majority of DSS-induced IBD-related genes which cover multiple genetic regulatory networks in IBD, and supplement of miR-146a mimics inhibited expression of many IBD-related genes. DOI 10.3389/fimmu.2024.1366319
2024-04-24 | GSE247433 | GEO
Project description:DSS-induced colitis aggravates gut microbiota dysbiosis and liver injury in mice with NASH
Project description:Aim: To assess the effect of IL-26 on mouse colonic tissue at steady state and in DSS-induced colitis through next-generation RNA sequencing of bulk RNA from colonic tissue. Results: We demonstrate an anti-inflammatory effect of IL-26 at both steady-state and after induction of DSS-colitis, through suppression of both cell recruitment and activation pathways.
Project description:Purpose : The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) of colon samples of intestinal epithelial cell specific Axin1 Knockout mice and WT controls that were submitted to DSS-induced colitis and AOM/DSS-induced colorectal carcinogenesis. Methods : DSS-induced colitis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice by giving 3% DSS dissolved in drinking water for 7 days and subsequently placed on regular water for recovery before sacrifice at Day 7 and D13. Methods : AOM/DSS-induced colorectal tumorigenesis was performed on Axin1flfl (WT) and Vil CreERT2;Axin1fl/fl (Axin1KOΔIEC) mice that were sacrificed at day 100 post-AOM injection to collect colorectal tumors. Methods : Colonic mRNA profiles of WT and Axin1KOΔIEC mice were generated by deep sequencing using Illumina NextSeq 500 instrument (150base-lengths read V2 chemistry in a paired-end mode)
Project description:To investigate whether the H3K27ac is involved in the development of inflammatory bowal disease. We established dextran sulfate sodium (DSS)-induced chronic colitis and performed RNA-sequencing and Chromatin Immunoprecipitation followed by NGS sequencing for H3K27ac in the mice colon tissues. We find that the global H3K27ac distribution in colon tissue had no significant difference, while on the typical-enhancers specific in the DSS group, H3K27ac signals were significantly enriched when compared with the control. Furthermore, we identified 89 candidate genes which represented the susceptible genes to H3K27ac change and predicted transcription factors (TFs) upon the DSS treatment. Collectively, our study revealed that H3K27ac increase on special typical-enhancers is possibly related to the development of intestinal inflammation by up-regulating adjacent gene expression and shifting TFs networks.
