Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from intestinal epithelium

ABSTRACT: Oxidative stress and celllular apoptosis of intestinal epithelial tissues relies on the environments from drinking different waters. In the rat intestinal epithelium, the toxic materials or antioxidant materials may affect the genes expression of oxidative stress and apoptosis through the oral intake ofa waters or agents. The up- or down-regulation in the antioxidant genes and apoptosis-related genes may represent the internal microenvironments in the intestine. Therefore, we used intestinal epithelium from rats drinking different waters to test the several genes expression. We used microarrays to detail the global programme of gene expression underlying damage or protection effect and identified distinct classes of up-regulated or down-regulated genes during drinking different waters test in this process.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE55142 | GEO | 2014/12/01

SECONDARY ACCESSION(S): PRJNA238623

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from YAP-S127A Villin-rtTA crypts

2012-11-29 | GSE41506 | GEO

Expression data from YAP-S127A Villin-rtTA crypts

Project description:We overexpressed YAP in the intestinal epithelium by adding doxycycline to the drinking water of experimental mice. Mice were given dox for 2 days, and referred to as Tg (transgenic). Mice were given dox for 2 days, sacrificed, and crypts were isolated for RNA extraction and analyzed by Affymetrix microarrays.

2012-11-29 | E-GEOD-41506 | biostudies-arrayexpress

Effects of caspase-8 deletion in the intestinal epithelium

Project description:Caspase-8 is a cystein protease involved in regulating apoptosis. The function of caspase-8 was studied in the intestinal epithelium, using mice with an intestinal epithelial cell specific deletion of caspase-8. We used microarrays to investigate the difference of the global programme of gene expression in intestinal epithelial cells of control and caspase-8 deficient mice. Intestinal epithelial cells were isolated from 3 control mice and 3 mice with a conditional deletion of caspase-8 in the intestinal epithelium. RNA was isolated and subjected to Affymetrix gene chip analysis.

2011-07-22 | E-GEOD-30873 | biostudies-arrayexpress

Genome-wide hydroxymethylcytosine pattern changes in response to oxidative stress

Project description:The TET-family enzymes (TETs) convert methylcytosine to hydroxymethylcytosine, a lately discovered epigenetic modification that can modulate transcription. While recent reports suggest that TETs may play a role in response to oxidative stress, this role remains uncertain. Here we show that Tet1 is sensitive to peroxide and report a global decrease in hydroxymethylcytosine in cells treated with BSO and in the intestinal epithelium of mice lacking the major antioxidant enzymes glutathione peroxidases 1 and 2. Furthermore, genome-wide profiling revealed differentially hydroxymethylated regions in genes involved in responses to oxidative stress. Intriguingly, a considerable proportion of these regions lie in genes encoding microRNAs predicted to target transcripts involved in oxidative stress response. This work thus demonstrates a profound effect of oxidative stress on the hydroxymethylome and opens exciting new avenues of research by highlighting a set of microRNAs that may participate in the prevention or etiology of oxidative-stress-related diseases. Examination of DNA hydroxymethylation landscape in SY5Y cell lines and in intestinal epithelium of mice.

2016-01-14 | E-GEOD-59718 | biostudies-arrayexpress

Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse

Project description:Methylation of H3K79 is associated with chromatin at expressed genes, though it is unclear if this histone modification is required for transcription of all genes. Recent studies suggest that Wnt-responsive genes depend particularly on H3K79 methylation, which is catalyzed by the methyltransferase DOT1L. Human leukemias carrying MLL gene rearrangements show DOT1L-mediated H3K79 methylation and aberrant expression of leukemogenic genes. DOT1L inhibitors reverse these effects but their clinical use is potentially limited by toxicity in Wnt-dependent tissues such as intestinal epithelium. Genome-wide positioning of the H3K79me2 mark in Lgr5+ mouse intestinal stem cells and mature intestinal villus epithelium correlated with mRNA expression levels but not with Wnt-responsive genes per se. Selective Dot1l disruption in Lgr5+ stem cells or in all intestinal epithelial cells eliminated H3K79me2 from the respective compartments, allowing genetic evaluation of DOT1L requirements. Absence of methylated H3K79 did not impair health, intestinal homeostasis or expression of Wnt target genes in crypt epithelium for up to 4 months, despite increased crypt cell apoptosis. Global transcript profiles in Dot1l-null cells were barely altered. Thus, H3K79 methylation is not essential for transcription of Wnt-responsive or other intestinal genes and intestinal toxicity is not imperative when DOT1L is rendered inactive in vivo. Examination of differential gene expression between Dot1l control (Dot1 f/f) and Dot1l mutant (Villin-Cre, Dot1l f/f) villus cells.

2012-10-19 | E-GEOD-41710 | biostudies-arrayexpress

Human cell toxicogenomic analysis links reactive oxygen species to the toxicity of monohaloacetic acid drinking water disinfection byproducts

Project description:The monohaloacetic acids (monoHAAs) are generated as byproducts during the disinfection of drinking water and are cytotoxic, genotoxic, mutagenic, and teratogenic. Iodoacetic acid (IAA) toxicity was mitigated by antioxidants, suggesting the involvement of oxidative stress. Other monoHAAs may share a similar mode of action. Human oxidative stress and antioxidant defense gene arrays (SA biosciences) were used to evaluate changes in transcriptome profiles in the human intestinal epithelial cell line FHS 74 INT generated by three compounds, chloroacetic acid (CAA), bromoacetic acid (BAA) and IAA at two time points (30 min and 4 h).

2013-08-11 | GSE49698 | GEO

Global gene expression analysis of Dot1l-deficient and control intestinal villus cells in mouse

2012-10-19 | GSE41710 | GEO

KAT2A and KAT2B prevents double-stranded RNA formation and interferon signaling to maintain intestinal stem cell renewal

Project description:Histone acetyltransferases KAT2A and KAT2B are paralogs highly expressed in the intestinal epithelium, but their functions are not well understood. In this study, double knockout of murine Kat2 genes in the intestinal epithelium was lethal, resulting in diminished H3K9ac expression, loss of stem cells, and robust activation of interferon signaling. Use of pharmacological agents and sterile organoid cultures indicated a cell-intrinsic double-stranded RNA trigger for interferon signaling. Acetyl-proteomics and dsRIP-seq were employed to interrogate the mechanism behind this response, which identified self-derived, mitochondria- encoded double-stranded RNA as the source of intrinsic interferon signaling. KAT2A and KAT2B therefore play an essential role in regulating mitochondrial functions as well as maintaining intestinal health.

2023-07-07 | MSV000092370 | MassIVE

Depletion of murine intestinal microbiota: effects on gut mucosa and epithelial gene expression

Project description:Inappropriate cross talk between mammals and their gut microbiota may trigger intestinal inflammation and drive extra-intestinal immune-mediated diseases. Studies with germ-free or gnotobiotic animals represent the gold standard for research on bacterial-host interaction but they are not readily accessible to the wide scientific community. We aimed at refining a protocol that in a robust manner would deplete murine intestinal microbiota and prove to have significant biologic validity. Previously published protocols for depleting mice of their intestinal microbiota by administering broad-spectrum antibiotics in drinking water were difficult to reproduce. We show that twice daily delivery of antibiotics by gavage depleted mice of their cultivable fecal microbiota and reduced the fecal bacterial DNA load by approximately 400 fold while ensuring the animals’ health. Mice subjected to the protocol for 17 days displayed enlarged ceca, reduced Peyer’s patches and small spleens. Antibiotic treatment significantly reduced the expression of antimicrobial factors and altered the expression of 517 genes in total in the colonic epithelium. Genes involved in cell cycle were significantly altered concomitant with reduced epithelial proliferative activity in situ assessed by Ki-67 expression, suggesting that commensal microbiota drives cellular proliferation in colonic epithelium. We present a robust protocol for depleting mice of their cultivatable intestinal microbiota with antibiotics by gavage and show that the biological effect of this depletion is phenotypic characteristics and epithelial gene expression profile similar to those of germ-free mice. Comparison of genome-wide gene expression of colon intestinal epithelial cells from mice subjected to microbiota depletion protocol against to control mice.

2011-08-14 | E-GEOD-22648 | biostudies-arrayexpress

Transcriptomic analysis of a gut epithelial cell line after the depletion of selenoprotein Glutathione peroxidase 4

Project description:GPx4 is an important antioxidant gene that is derived from selenium. A ploymorphism in GPx4 has been associated with increased risk of colorectal and prostate cancer. This experiment decsribes the effect of change in GPx4 expression in human intestinal epithelial cell line (Caco-2).Depletion of GPx4 expression led to changes in mitochondrial pathways including oxidative phosphorylation and ubiquinone biosynthesis pathway and genes involved in apoptosis regulation

2013-01-01 | GSE40287 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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