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Murine small intestinal crypt cell line IEC-6: control vs. TGF-beta stimulated

ABSTRACT: microRNA profiling of rat small intestinal crypt cell IEC-6. Comparing control untreated with cells treated with transforming growth factor-beta (TGF-beta). TGF-beta stimulated cell differentiation, as observed in the stimulation of intestinal epithelial cell markers (alkaline phophotase, villin, aminopeptidase N, etc.).

ORGANISM(S): Mus musculus Human gammaherpesvirus 8 Rattus norvegicus Human alphaherpesvirus 1 JC polyomavirus Betapolyomavirus macacae Homo sapiens Human immunodeficiency virus 1 Murid gammaherpesvirus 4 Human betaherpesvirus 5 Betapolyomavirus hominis human gammaherpesvirus 4 Murid betaherpesvirus 1

PROVIDER: GSE20982 | GEO | 2012/06/19

SECONDARY ACCESSION(S): PRJNA124489

REPOSITORIES: GEO

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Murine small intestinal crypt cell line IEC-6: control vs. TGF-beta stimulated

Project description:microRNA profiling of rat small intestinal crypt cell IEC-6. Comparing control untreated with cells treated with transforming growth factor-beta (TGF-beta). TGF-beta stimulated cell differentiation, as observed in the stimulation of intestinal epithelial cell markers (alkaline phophotase, villin, aminopeptidase N, etc.). Two condition experiment. Control vs TGF-beta treatment. Biological replicates: 3 control, 3 treated. Independently grown and harvested. One replicate per array

2012-06-18 | E-GEOD-20982 | biostudies-arrayexpress

RNA-seq of crypt and villus cells from mouse small intestinal epithelium with an intestinal-epithelial specific deletion of LSD1 compared to wild type controls

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ZIP7 is indispensable for proliferation of intestinal epithelial cells and maintenance of intestinal stem cells

Project description:Intestinal epithelium are generated by intestinal stem cells, which are recognized morphologically as slender columnar cells at the base of the crypt. Stem cells produce transit-amplifying (TA) cells, which divide a number of times and the daughter cells differentiate into absorptive enterocytes as well as secretory-lineages. Intestinal stem cells highly express Lgr5 which is decreased in TA cells. Here, we show that the zinc transported SLC39A7/ZIP7 is essential for the proliferation of TA cells and maintenance of intestinal stem cells. Lgr5Med TA cells derived from Zip7-deficient mice upregulated the expression of unfold protein responses-related genes including pro-apoptotic genes, indicating of induction of ER stress in these cells. The same effect was seen in Lgr5Hi stem cells derived from Zip7-deficient mice. We conclude that ZIP7 is fundamental to the maintenance of crypt homeostasis by resolving ER stress. Small intestinal crypts were isolated form tamoxifen-treated control (Zip7flox/+, Villin-CreERT2, Lgr5-EGFP-ires-CreERT2) and tamoxifen-treated Zip7â??IEC (Zip7flox/flox, Villin-CreERT2, Lgr5-EGFP-ires-CreERT2) mice. We FACS purified intestinal crypt cells according to their Lgr5 expression levels. RNA was isolated from four FACS sorted cell populations: Lgr5Hi cells and Lgr5Med cells derived from control mice, Lgr5Hi cells and Lgr5Med cells derived from Zip7â??IEC mice. Isolated RNA was analyzed using the Affymetrix platform.

2016-08-19 | E-GEOD-72190 | biostudies-arrayexpress

RNA-seq of crypt and villus cells from small intestinal epithelium from mice treated with antibiotics with an intestinal-epithelial specific deletion of LSD1 compared to wild type

Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts and villus from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (cKO) (Villin-Cre+; Lsd1f/f) mice. This experiment uses a new Cre strain with 100% recombination efficiency. RNA was directly isolated from the crypt and villus, and this was used for RNAseq. Gene expression analysis of cKO derived crypt and villus provides a spatially restricted outlook on the maturation status of the intestinal epithelium in the villi and the absence of Paneth cells in the crypt. Additionally, these mice were treated with antibiotics to study epithelium intrinsic changes related to LSD1 deletion but independent of the bacterial microbiome.

2023-08-02 | E-MTAB-10499 | biostudies-arrayexpress

Rattus norvegicus

Project description:Murine small intestinal crypt cell line IEC-6: control vs. TGF-beta stimulated

| PRJNA124489 | ENA

The effect of TGF-beta in Apc-mutated mouse intestinal organoids

Project description:Intestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta. Total RNA obtained from Tamoxifen-treated, Apc-deleted intestinal organoids in the absence or presence of 3 ng/ml TGF-beta (18h).

2014-04-18 | E-GEOD-35093 | biostudies-arrayexpress

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

Project description:To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells Total RNA was prepared from enterocytes obtained from small intestines of IKKb(EE)IEC and WT littermates. Two biological replicates were performed for each experimental condition.

2011-06-09 | E-GEOD-29701 | biostudies-arrayexpress

RNA-seq of crypt cells from mouse small intestinal epithelium with an intestinal-epithelial specific deletion of LSD1 compared to wild type crypts

Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We dissociated crypts into single cells, and FACS sorted Epcam+ cells, to avoid immune-cell contamination. RNA was directly isolated from these sorted cells, and this was used for RNA seq. As KO crypts are different from WT crypts (KO crypts lack Paneth cells), identifying genes specifically regulated by LSD1 helps us to identify how LSD1 regulates intestinal crypt biology. Specifically, because we were able to combine this with ChIP-seq of the same cells, to identify where H3K4me1 levels (target of the histone demethylase LSD1) were different in the genome.

2020-11-16 | E-MTAB-7862 | biostudies-arrayexpress

IKKα promotes intestinal tumorigenesis

Project description:Depending on the tumor type IκB kinase α (IKKα) can act as tumor promoter or tumor suppressor in various malignancies. Here we demonstrate a key function of IKKα in the suppression of a tumoricidal microenvironment during intestinal carcinogenesis. Mice deficient in IKKα kinase activity are largely protected from intestinal tumor development that is dependent on the enhanced recruitment of IFNγ expressing M1-like myeloid cells. In IKKα mutant mice M1-like polarization is not controlled in a cell autonomous manner but depends rather on the interplay of both IKKα mutant tumor epithelia and immune cells. Tamoxifen-inducible β-catc.a. mice comprise an excellent model to study Wnt-dependent tumor initiation. These mice are characterized by IEC-restricted stabilization of β-catenin causing rapid expansion of intestinal crypts and loss of differentiated IEC. To further explore the underlying IKKα controlled pro-proliferative mechanism, we performed a microarray analysis comparing RNA isolated from wildtype, IkkαAA/AA, β-catc.a. or β-catc.a./IkkαAA/AA IEC 15 days after the first tamoxifen administration. and within 4 weeks β-catc.a. mice succumb to this marked crypt hyperproliferation

2014-06-01 | E-GEOD-51631 | biostudies-arrayexpress

Spatial tissue proteomics analysis of laser capture microdisscted intestinal crypt compartment

Project description:Crypt hyperplasia is a key feature of celiac disease and various other small intestinal inflammatory conditions. By undertaking mass spectrometry-based tissue proteomics of the gut epithelial crypt zone, we found that active celiac disease is characterized by a strong interferon-γ (IFN-γ) signal. This signal, hallmarked by increased expression of MHC molecules, coincides with a markedly reduced expression of proteins associated with fatty acid metabolism. We observed similar crypt hyperplasia and proteomic alterations in wild-type mice treated with IFN-γ, but not in mice that lack the IFN-γ receptor in gut epithelial cells. IFN-γ is thus a driver of crypt hyperplasia in celiac disease by acting directly on crypt epithelial cells. This dataset contains proteomics analysis of crypt compartment samples isolated by laser capture microdissection small intestinal crypt compartment from C57/Bl6 mice injected i.p. with 0-1-2-4-6 or 9 doses interferon gamma every 8 hour.

2025-08-08 | PXD062684 | Pride

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