Project description:Selected brain regions of mice with chronic DSS colitis and controls, and mice with colitis caused by induced, intestinal epithelial-specific Opa1 knock-out to study the impact of gut inflammation on the brain
Project description:Whole right brain hemispheres of mice with adaptive T-cell transfer colitis and controls to study the impact of gut inflammation on the brain
Project description:Whole right brain hemispheres of mice with Citrobacter rodentium infection-induced colitis and controls to study the impact of gut inflammation on the brain
Project description:Whole right brain hemispheres of mice with colitis caused by induced, intestinal epithelial-specific Opa1 knock-out to study the impact of gut inflammation on the brain
Project description:Background: MicroRNAs (miRNAs) acting as negative regulators of gene expression are differentially expressed in intestinal tissues of patients with inflammatory bowel disease (IBD). Assessing the functional role of miRNAs in murine models of colitis facilitates elucidating the role of specific miRNAs in human IBD. The aim of this study was to determine the miRNA signature of murine models of colitis and to assess the influence of miR-21 on intestinal inflammation. Methods: miRNAs expression was accessed by microarray for acute and chronic murine model of colitis induced by DSS or TNBS. miR-21-deficient mouse and littermates controls were assessed in the standard DSS, TNBS and CD4+ T cell transfer models of colitis. RNAs of mouse colon and CD4+CD45RBHigh cells were analyzed by miRNA and mRNA microarray, and quantitative RT-PCR. Th1 polarization was accessed by flow-cytometry and ELISA. Results: Alterations of in miRNAs expression were identified for acute and chronic DSS colitis and TNBS colitis, receptively. The Expression of miRs-21, -142-3p and -223 was were distinct between DSS and TNBS models while overlap of numerous miRNAs was seen. Importantly, miRs-19b, -192 and -215, that are decreased in IBD, were significantly decreased in all 4 models of colitis. miR-21, which is increased in IBD, was increased in TNBS colitis but not the DSS colitis models. Further assessment of the miR-21-deficient 1-/- mice revealed that the deletion of miR-21 results in the exacerbation of both the TNBS and T cell-transfer models of colitis. Conclusions: miRNAs are differentially expressed in both human IBD and murine colitis, with overlap of several IBD-associated miRNAs. The demonstration that miR-21 deletion exacerbated CD4+ T cell-mediated models of colitis provides further evidence that miRNAs play significant roles in the pathogenesis of IBD. miRNAs expression was accesed for acute and chronic murine model of colitis induced by DSS or TNBS.Total of 20 samples with duplicates were analyed in this study.
Project description:Part of a mouse inflammation model set in order to observe the similarities and differences between the multiple options for the generation of intestinal inflammation in an animal model. Experimental samples are generated according to the standard protocol for the model and are processes using the same set of bioinformatic tools.
Project description:This experiment investigates transcriptional changes in whole blood during the recovery phase of dextran sulfate sodium (DSS)-induced colitis in mice, with or without treatment by synthetic mucin polymers (Shear-Labile Interaction Polymers, SLIPs). DSS (2.5% w/v) was administered for four days to induce acute epithelial injury, followed by four days of recovery in which mice received either water (control) or SLIPs (6.66 mg/mL) in drinking water. Whole-blood clots were collected on day 8 and processed for RNA extraction using a modified TRIzol LS protocol adapted for frozen clots. Libraries were prepared and sequenced on an Illumina NovaSeq 6000 platform (paired-end 150 bp). Differential expression analysis compared SLIP-treated and untreated groups to identify genes involved in immune regulation, redox balance, and epithelial recovery following colitis.
Project description:To understand the role of ATF6a and ATF6b in non-canonical endoplasmic reticulum stress response pathway, we have employed whole genome microarray expression profiling to identify the genes regulated by ATF6s. WIild type or, ER stress mediators,ATF6a or ATF6b-knockout mice were treated with 3% DSS for 3days. Genes responsible for DSS in each mediator-dependent manner were extracted and categorized by Gene Ontology. Among them, expression of three cell structure-related genes (Muc2, Muc3, Muc4) was quantified in the RNA samples from another mice treated with DSS by real-time PCR. Colitis was induced with 3% DSS, 36,000-50,000 M.W. (MP Biomedicals,) in the drinking water for 3 days. Genes responsible for DSS treatment in each mediator-dependent manner were extracted and categorized by Gene Ontology in GeneRanker program of Genomatix platform.