Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of whole-blood clots from DSS-induced colitis mice treated with Shear-Labile Interaction Polymers (SLIPs)

ABSTRACT: 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.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER: Luiz Roesch

PROVIDER: E-MTAB-16067 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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RNA-seq of whole-blood clots from DSS-induced colitis mice treated with Shear-Labile Interaction Polymers (SLIPs)

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