Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigating the Interleukin-22 regulated transcriptome in normal and APC-mutant small intestinal epithelial organoids

ABSTRACT: Purpose: to investigate the effects of the cytokine Interluekin-22 (IL-22) on small intestinal epithelial cells, using organoids. Methods: WT or Apc(Min/Min) organoids (day 3) were stimulated with IL-22 (2ng/ml) for 3 hours, and submitted for transcriptomic profiling. Results: The main function of IL-22 in small intestinal epithelial cells is to activate an antimicrobial immune response and defence against infection and stress. Further, we found that loss of Apc lead to a complete loss of response to IL-22

ORGANISM(S): Mus musculus

PROVIDER: GSE139332 | GEO | 2019/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Investigating the Interleukin-22 regulated transcriptome in normal and APC-mutant small intestinal epithelial organoids

Project description:Investigating the Interleukin-22 regulated transcriptome in normal and APC-mutant small intestinal epithelial organoids

| PRJNA579334 | 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

Mouse intestinal crypt epithelial cells: Apc+/Î716 mice vs. Apc+/Î716 Id2-/- compound mutant mice

Project description:Transcriptional profiling of mouse intestinal crypt epithelial cells comparing Apc+/Î716 mice with Apc+/Î716 Id2-/- mice. One-condition experiment, Apc+/Î716 mice vs. Apc+/Î716 Id2-/- mice, Biological replicates: 1 pooled intestinal crypt epithelium from 3 Apc+/Î716 mice, 1 pooled intestinal crypt epithelium from 3 Apc+/Î716 Id2-/- mice. One replicate per array.

2016-03-01 | E-GEOD-66480 | biostudies-arrayexpress

Lipid Profiling of Mouse Intestinal Organoids for studying APC Mutations

Project description:Inactivating mutations including both germline and somatic mutations in the adenomatous polyposis coli (APC) gene drives most familial and sporadic colorectal cancers. Understanding the metabolic implications of this mutation will aid to establish its wider impact on cellular behaviour and potentially inform clinical decisions. However, to date, alterations in lipid metabolism induced by APC mutations remain unclear. Intestinal organoids have gained widespread popularity in studying colorectal cancer and chemotherapies, because their three-dimensional structure more accurately mimics an in vivo environment. Here, we aimed to investigate intra-cellular lipid disturbances induced by APC gene mutations in intestinal organoids using a reversed-phase ultra-high-performance liquid chromatography mass spectrometry (RP-UHPLC-MS)-based lipid profiling method. Lipids of the organoids grown from either wildtype (WT) or mice with Apc mutations (Lgr5–EGFP-IRES-CreERT2 Apcfl/fl) were extracted and analysed using RP-UHPLC-MS. Concentrations of phospholipids (e.g. PC(16:0/16:0), PC(18:1/20:0), PC(38:0), PC(18:1/22:1)), ceramides (e.g. Cer(d18:0/22:0), Cer(d42:0), Cer(d18:1/24:1)) and hexosylceramide (e.g. HexCer(d18:1/16:0), HexCer(d18:1/22:0)) were higher in Apcfl/fl organoids, whereas levels of sphingomyelins (e.g. SM(d18:1/14:0), SM(d18:1/16:0) ) were lower compared to WT. These observations indicate that cellular metabolism of sphingomyelin was upregulated, resulting in the cellular accumulation of ceramides and production of HexCer due to the absence of Apcfl/fl in the organoids. Our observations demonstrated lipid profiling of organoids and provided an enhanced insight into the effects of the APC mutations on lipid metabolism, making for a valuable addition to screening options of the organoid lipidome.

2021-02-17 | ST001707 | MetabolomicsWorkbench

Gene expression changes in Apc-mutant mouse intestinal organoids with and without deleting the Prox1 transcription factor

Project description:We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen. Total RNA obtained from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox organoids were compared 7 days after the addition of tamoxifen and 5 days after the selection for Apc-mutant organoids in the absence of the Wnt-agonist R-Spondin1.

2014-08-15 | E-GEOD-47568 | biostudies-arrayexpress

Mouse intestinal crypt epithelial cells: Apc+/Δ716 mice vs. Apc+/Δ716 Id2-/- compound mutant mice

Project description:Transcriptional profiling of mouse intestinal crypt epithelial cells comparing Apc+/Δ716 mice with Apc+/Δ716 Id2-/- mice.

2016-03-01 | GSE66480 | GEO

Gene expression changes in Apc-mutant mouse intestinal organoids 7 and 20 days after the induction of the Apc deletion

Project description:We isolated and selected intestinal adenoma organoids from Lgr5-EGFP-IRES-CreER; Apcflox/flox mice and added tamoxifen to induce the deletion of the Apc gene in the intestinal stem cells. Gene expressions on day7 and day20 after the addition of tamoxifen were compared, representing two stages with different colorectal cancer stem cell content. Total RNA obtained from Lgr5-EGFP-IRES-CreER; Apcflox/flox organoids were compared 7 days and 20 days after the addition of tamoxifen, cultured without the Wnt-agonist R-Spondin1.

2015-12-31 | E-GEOD-47569 | biostudies-arrayexpress

RNA-Seq as part of a study to investigate impact of Atg16l on Il22 signalling in the intestinal mucosa

Project description:A coding variant of the inflammatory bowel disease (IBD) risk gene ATG16L1 has been associated with defective autophagy and deregulation of endoplasmic reticulum (ER) function. IL-22 is a barrier protective cytokine by inducing regeneration and antimicrobial responses in the intestinal mucosa. We show that ATG16L1 critically orchestrates IL-22 signaling in the intestinal epithelium. IL-22 stimulation physiologically leads to transient ER stress and subsequent activation of STING dependent type I interferon (IFN-I) signaling, which is augmented in Atg16l1ΔIEC intestinal organoids. IFN-I signals amplify epithelial TNF production downstream of IL-22 and contribute to necroptotic cell death. In vivo, IL-22 treatment in Atg16l1ΔIEC and Atg16l1ΔIEC/Xbp1ΔIEC mice potentiates endogenous ileal inflammation and causes widespread necroptotic epithelial cell death. Therapeutic blockade of IFN-I signaling ameliorates IL-22 induced ileal inflammation in Atg16l1ΔIEC mice. Our data demonstrate an unexpected role of ATG16L1 in coordinating the outcome of IL-22 signaling in the intestinal epithelium.

2018-09-18 | GSE119354 | GEO

Non-tumor/tumor intestinal tissue of control or intestine-specific HAI-1 deficient Apc(Min/+) mice

Project description:To analyse roles of HAI-1/Spint1 in intestinal tumorigenesis, we examined the effect of intestine-specific deletion of Spint1 gene on Apc(Min/+) mice. The loss of Hai-1/Spint1 significantly accelerated tumor formation in ApcMin/+ mice and shortened their survival periods. Mouse small intestine tumor tissue or background mucosa lacking macroscopically visible tumors were proceeded to RNA extraction and hybridization on microarrays (Affymetrix Mouse Genome 430 2.0 Array). Non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox) mice and non-tumor or tumor intestinal mucosa tissues of Apc (Min/+)/Spint1 (flox/flox)/Vil-Cre mice were analysed. The experiment was repeated respectively.

2013-04-01 | E-GEOD-40856 | biostudies-arrayexpress

microRNAs differentially regulated in organoids derived from tumors of Apc-deficient mice

Project description:microRNA expression profiles were investigated in organoids derived from tumors of Apc-deficient mice and normal intestinal epitehlia of wild-type mice.

2016-12-01 | GSE75482 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data