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
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)
