Mus musculus
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ABSTRACT:
PROVIDER: PRJNA306526 | ENA |
REPOSITORIES: ENA
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Project description:Whole transcriptome analysis of functionally distinct cell types of the jejunal intestinal epithelium of germfree and conventionalized mice [mRNA]
| PRJNA320645 | ENA
Project description:Whole transcriptome analysis of functionally distinct cell types of the jejunal intestinal epithelium of germfree and conventionalized mice
| PRJNA320643 | ENA
Project description:mRNA sequencing of small intestinal tissue of germfree mice
| PRJNA257651 | ENA
Project description:The goal of the present study was to determine whether loss of the insulin receptor alters the molecular landscape of the intestinal mucosa, using intestinal-epithelial insulin receptor knockout (IE-irKO) mice and both genetic (IRfl/fl and Villin-cre) controls. Quantitative proteomic analysis by Liquid Chromatography Mass Spectrometry (LC-MS) was deployed on jejunal and colonic mucosa from mice fed a chow- or Western diet (WD). Jejunal mucosa from IE-irKO mice demonstrated alterations in all intestinal cell linages, Paneth, goblet, absorptive and enteroendocrine cells, whereas only goblet and absorptive cells were affected in the colon. There was also a significant effect of the WD on the gut proteome. A significant reduction was detected in Paneth cell proteins with anti-microbial activity, including lysozyme C-1, angiogenin-4, cryptdin-related sequence1C-3 and -2, a-defensin 17 and intelectin-1a. The key protein expressed by goblet cells, mucin-2, was also reduced in the IE-irKO mice. Proteins involved in lipid metabolism, including aldose reductase-related protein 1, 15-hydroxyprostaglandin dehydrogenase [NAD(+)], apolipoprotein A-II and pyruvate dehydrogenase kinase isozyme 4, were increased in the mucosa of WD-fed IE-irKO mice as compared to controls. In contrast, expression of the nutrient-responsive gut hormones, glucose-dependent insulinotropic polypeptide and neurotensin, was reduced in the jejunal mucosa of IE-irKO mice, and there was a reduction in proteins of the P-type ATPases and the solute carrier-transporter family in the colon of WD-fed IE-irKO mice. In conclusion, IE-irKO mice display a distinct molecular phenotype, suggesting a biological role of insulin and its receptor in determining differentiated cell-specificity in the intestinal epithelium.
2017-08-18 | PXD005932 | Pride
Project description:We profiled transcriptome and chromatin landscapes in jejunal mouse intestinal epithelial cells (IECs) from mice reared in the absence (Germ Free or GF) or presence (Conventionalized or CV) of microbiota. We show that microbiota colonization results in changes in histone modifications at hundreds of enhancers that are associated with microbiota-regulated genes. Furthermore, we show that microbiota colonization is associated with a drastic genome-wide reduction in Hnf4a and Hnf4g binding.
2017-03-27 | GSE90461 | GEO
Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we grew small intestinal organoids in vitro from mice with an epithelial specific deletion of LSD1 (Villin-Cre+; Lsd1f/f) and from wild type (Villin-Cre-; Lsd1f/f) mice. This experiment uses a new Cre strain with 100% recombination efficiency. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, Paneth cells are not present in LSD1-KO small intestinal organoids. We used these sequencing data to show intrinsic epithelial changes in the intestinal epithelium caused by LSD1 deletion in the absence of microbiota and surrounding in vivo cell types.
2023-08-02 | E-MTAB-10500 | biostudies-arrayexpress
Project description:RNA-seq of isolated zebrafish enteroendocrine cells and other intestinal epithelium cells from germ-free (GF) and conventionalized (CV) zebrafish
2020-06-04 | GSE151711 | GEO
Project description:Obesity is associated with an increased risk of mucosal infections; however, the mechanistic basis of this phenomenon remains incompletely defined. Intestinal mucus barrier systems normally prevent infections, but are sensitive to changes in the luminal environment. Here we demonstrate that mice exposed to an obesogenic Western-style diet (WSD) suffer regiospecific failure of the mucus barrier in the small intestinal jejunum caused by diet-induced mucus condensation, which occurs independently of microbiota alterations. Mucus barrier disruption due to either WSD exposure or chromosomal Muc2 deletion results in collapse of the commensal jejunal microbiota, which in turn sensitises mice to atypical jejunal colonization by the enteric pathogen Citrobacter rodentium. We identify the jejunal mucus layer as a microbial habitat, and link the regiospecific mucus dependency of the microbiota to fundamental properties of the jejunal niche. Together, our data identifies a symbiotic mucus-microbiota relationship that normally prevents jejunal pathogen colonization, but is highly sensitive to disruption by exposure to a Western-style diet.
2023-05-12 | PXD028613 | Pride
Project description:Mitochondrial dysfunction is associated with inflammatory bowel diseases (IBD). To understand how microbial-metabolic circuits contribute to intestinal tissue injury, we disrupt mitochondrial function in the intestinal epithelium by deleting heat shock protein 60 (Hsp60Δ/ΔIEC). While metabolic perturbation causes self-resolving tissue injury, regeneration is disrupted in the absence of aryl hydrocarbon receptor (Hsp60Δ/ΔIEC;AhR-/-) or IL-10 (Hsp60Δ/ΔIEC;Il10-/-) leading to IBD-like pathology. Tissue pathology is absent in the distal colon of germfree (GF) Hsp60Δ/ΔIEC mice, highlighting bacterial control of metabolic injury. Selective colonization of GF Hsp60Δ/ΔIEC mice with the synthetic community OMM12 confirms expansion of metabolically-flexible Bacteroides ssp., which generates metabolic injury in mono-colonized mice. Transcriptional profiling of metabolically-impaired epithelium identifies gene signatures, such as Ido1, Nos2, and Duox2, differentiating active from inactive tissue inflammation in 343 tissue sections from Crohn’s disease patients. In conclusion, mitochondrial perturbation of the epithelium causes microbiota-dependent tissue injury and discriminative inflammatory gene profiles with relevance for IBD.
2024-07-15 | PXD052829 | Pride
Project description:Background and Aims: Although the zinc finger transcription factor GATA4 has been implicated in regulating jejunal gene expression, the contribution of GATA4 in controlling jejunal physiology has not been addressed. Methods: We generated mice in which the Gata4 gene was specifically deleted in the small intestinal epithelium. Measurements of plasma cholesterol and phospholipids, intestinal absorption of dietary fat and cholesterol, and gene expression were performed on these animals. Results: Mice lacking GATA4 in the intestine displayed a dramatic block in their ability to absorb cholesterol and dietary fat. Comparison of the global gene expression profiles of control jejunum, control ileum, and GATA4 null jejunum by gene array analysis demonstrated that GATA4 null jejunum lost expression of 53% of the jejunal-specific gene set and gained expression of 47% of the set of genes unique to the ileum. These alterations in gene expression included a decrease in mRNAs encoding lipid and cholesterol transporters as well as an increase in mRNAs encoding proteins involved in bile acid absorption. Conclusion: Our data demonstrate that GATA4 is essential for jejunal function including fat and cholesterol absorption and confirm that GATA4 plays a pivotal role in determining jejunal versus ileal identity. Keywords: genetic modification
2008-09-01 | GSE11194 | GEO