Project description:Folic acid supplementation (8 mg/kg diet) promotes colon tumor formation in mice with established colitis induced by carcinogen azoxymethane (AOM) and dextran sulfate sodium sulfate (DSS). This induction of colon tumors was associated with hypomethylation of DNA cased by folic acid supplementation.
Project description:Folic acid supplementation (8 mg/kg diet) promotes colon tumor formation in mice with established colitis induced by carcinogen azoxymethane (AOM) and dextran sulfate sodium sulfate (DSS). This induction of colon tumors was associated with hypomethylation of DNA cased by folic acid supplementation.
Project description:The goal of the experiment was to compare the liver transcriptional profile of wild-type and IL-10 knockout mice with colitis. Colitis was induced in 6 week old female wild-type and IL-10-deficient C57BL/6 mice by administration of 3% dextran sulfate sodium (DSS) in the drinking water for 7 days. At necropsy, segments of liver were homogenized in Trizol and total RNA prepared for the transcriptional profiling.
Project description:The goal of the experiment was to compare the liver transcriptional profile of wild-type and IL-10 knockout mice with colitis. Colitis was induced in 6 week old female wild-type and IL-10-deficient C57BL/6 mice by administration of 3% dextran sulfate sodium (DSS) in the drinking water for 7 days. At necropsy, segments of liver were homogenized in Trizol and total RNA prepared for the transcriptional profiling. Total RNA from 4 wild-type and 4 IL-10 knockout mice with colitis was used to hybridize to Affymetrix Gene Chip Mouse 2.0 ST arrays.
Project description:Dual-specificity phosphatase 6 (Dusp6)-deficiency enhances baseline colon barrier integrity and confers amelioration of dextran sulfate sodium (DSS)-induced colonic injury. DUSP6 is a phosphatase, and therefore it is plausible that DUSP6 knockout alters the phosphorylation status of other proteins. To access the protein phosphorylation landscape and functional network in DUSP6 deficient Caco-2 cells, we applied phosphopeptide enrichment and isobaric labeling strategies with MS-based proteomics, and identified 1323 phosphorylation sites on 580 phosphoproteins.
Project description:To investigate the potential role of Dectin-1 in the development of intestinal tumorigenesis, we used Dectin-1 deficient (Clec7a–/–, KO) mice under germ-free (GF) condition and azoxymethane (AOM) and 3 cycles of dextran-sodium-sulfate (DSS)-induced mouse colorectal tumor model to compare with wild-type (WT) mice.
Project description:Wild type (WT), Nod2-/-, Pglyrp3-/-, and Pglyrp3-/-Nod2-/- mice (BALB/c) were treated with oral 5% dextran sodium sulfate (DSS) for 48, 72, or 96 hrs, their colons were removed and homogenized, and RNA was isolated using the TRIZOL method. Quantitative reverse transcription real-time PCR (qRT-PCR) was used to quantify the amounts of mRNA in the colon using the inflammatory gene expression RT2 Profiler PCR Array from Qiagen/SA Biosciences.
Project description:Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice are all more sensitive than wild type (WT) mice to dextran sulfate sodium (DSS)-induced colitis. The purpose of this study was to determine which genes are differentially induced by DSS treatment in the colon of Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice compared to WT mice. The results demonstrate higher induction of proinflammatory gene expression in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice than in WT mice after DSS treatment. The majority of genes whose expression is increased in Pglyrp1-/-, Pglyrp2-/-, Pglyrp3-/-, and Pglyrp4-/- mice but not in WT mice are interferon-inducible genes. Thus, Peptidoglycan Recognition Proteins Pglyrp1, Pglyrp2, Pglyrp3, and Pglyrp4 protect mice from excessive inflammatory response and damage to the colon by limiting expression of interferon-inducible genes in the colon.
Project description:In order to understand the molecular changes associated with the establishment of the repairing epithelium following dextran sulfate sodium (DSS) induced injury of the colon we have isolated Epcam+Sca1+ expressing epithelial cells from repairing tissue and Epcam+ homeostatic intestine. Cells isolated by flow cytometry were subjected to RNA extraction and analysed by expression analysis
Project description:Wild type (WT), Nod2-/-, Pglyrp3-/-, and Pglyrp3-/-Nod2-/- mice (BALB/c) were treated with oral 5% dextran sodium sulfate (DSS) for 48, 72, or 96 hrs, their colons were removed and homogenized, and RNA was isolated using the TRIZOL method. Quantitative reverse transcription real-time PCR (qRT-PCR) was used to quantify the amounts of mRNA in the colon using the inflammatory gene expression RT2 Profiler PCR Array from Qiagen/SA Biosciences. qRT-PCR gene expression profiling
