Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of nouse TNBS-induced murine colitis

ABSTRACT: We investigated the relationship between chronic inflammation and fibrosis in a mouse model of chronic colitis. Six weekly Trinitrobenzenesulphonic acid (TNBS) enemas were given to establish colitis and temporal changes in gene expression was elucidated over the next six weeks. Experiment Overall Design: After the six TNBS enemas, mice were sacrificed at 3 days (termed as TNBS-w6, n=6), 2 weeks (TNBS-w8, n=4), 4 weeks (TNBS-w10, n=5), or 6 weeks (TNBS-w12, n=4). The saline control groups were also sacrificed at week 6 (Saline-w6, n=5), week 8 (n=2) and week 10 (n=2). The last two sets were pooled as Saline-w10 (n=4). Two replicates of saline-w6 were analyzed. We compared Saline-w6 with TNBS-w6, and Saline-w10 with TNBS-w8, TNBS-w10, TNBS-w12, respectively.

ORGANISM(S): Mus musculus

SUBMITTER: Shukti Chakravarti

PROVIDER: E-GEOD-5864 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Differential expression of inflammatory and fibrogenic genes and their regulation by NF-kappaB inhibition in a mouse model of chronic colitis.

Wu Feng F Chakravarti Shukti S

Journal of immunology (Baltimore, Md. : 1950) 20071101 10

Fibrosis is a major complication of chronic inflammation, as seen in Crohn's disease and ulcerative colitis, two forms of inflammatory bowel diseases. To elucidate inflammatory signals that regulate fibrosis, we investigated gene expression changes underlying chronic inflammation and fibrosis in trinitrobenzene sulfonic acid-induced murine colitis. Six weekly 2,4,6-trinitrobenzene sulfonic acid enemas were given to establish colitis and temporal gene expression patterns were obtained at 6-, 8-, ...[more]

PMID: 17982090

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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.

Dataset Information

Transcription profiling of nouse TNBS-induced murine colitis

Publications

Differential expression of inflammatory and fibrogenic genes and their regulation by NF-kappaB inhibition in a mouse model of chronic colitis.

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