Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RRBS]

ABSTRACT: Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RRBS]

PROVIDER: PRJNA684493 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13241981.fastq.gz	Fastqsanger.gz
	SRR13241982.fastq.gz	Fastqsanger.gz
	SRR13241983.fastq.gz	Fastqsanger.gz
	SRR13241984.fastq.gz	Fastqsanger.gz
	SRR13241985.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model

Project description:Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model

| PRJNA684486 | ENA

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RNA-Seq]

Project description:Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RNA-Seq]

| PRJNA684491 | ENA

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RRBS]

Project description:Epigenetic dysregulation is likely to play a role in the observed association between inflammatory bowel disease (IBD) and colon tumor development. In the present work, DNA methylome, hydroxymethylome, and transcriptome analyses were conducted in proximal colon tissues harvested from the Helicobacter hepaticus-infected murine model of IBD. Reduced representation bisulfite sequencing (RRBS) and oxidative RRBS (oxRRBS) analyses identified 1606 differentially methylated regions (DMR) and 3011 differentially hydroxymethylated (DhMR) regions. These DMR/DhMR overlapped with genes that are associated with gastrointestinal disease, inflammatory disease, and cancer. RNA-seq revealed pronounced expression changes of a number of genes associated with inflammation and cancer. Several genes (e.g. Duox2, Tgm2, Cdhr5, Hk2) exhibited both changes in DNA methylation/ hydroxymethylation and altered gene expression levels. Overall, our results suggest that chronic inflammation triggers changes in methylation and hydroxymethylation patterns in the genome, altering the expression of key tumorigenesis genes and potentially contributing to the initiation of colorectal cancer.

2021-01-11 | GSE163037 | GEO

Multi-Omics Characterization of Inflammatory Bowel Disease-Induced Hyperplasia/Dysplasia in the Rag2-/-/Il10-/- Mouse Model.

Project description:Epigenetic dysregulation is hypothesized to play a role in the observed association between inflammatory bowel disease (IBD) and colon tumor development. In the present work, DNA methylome, hydroxymethylome, and transcriptome analyses were conducted in proximal colon tissues harvested from the Helicobacter hepaticus (H. hepaticus)-infected murine model of IBD. Reduced representation bisulfite sequencing (RRBS) and oxidative RRBS (oxRRBS) analyses identified 1606 differentially methylated regions (DMR) and 3011 differentially hydroxymethylated regions (DhMR). These DMR/DhMR overlapped with genes that are associated with gastrointestinal disease, inflammatory disease, and cancer. RNA-seq revealed pronounced expression changes of a number of genes associated with inflammation and cancer. Several genes including Duox2, Tgm2, Cdhr5, and Hk2 exhibited changes in both DNA methylation/hydroxymethylation and gene expression levels. Overall, our results suggest that chronic inflammation triggers changes in methylation and hydroxymethylation patterns in the genome, altering the expression of key tumorigenesis genes and potentially contributing to the initiation of colorectal cancer.

| S-EPMC7795000 | biostudies-literature

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-11 | GSE163038 | GEO

Multi-omics characterization of inflammatory bowel disease induced hyperplasia/dysplasia in the Rag2-/- / Il10-/- mouse model [RNA-Seq]

2021-01-11 | GSE163036 | GEO

Expression data of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors

Project description:Expression profiling of Rag2-deficient Ets1++ and Rag2-deficient Ets1-- mature NK cells and WT bone marrow progenitors, WT T cells, and WT Pro B cells

2012-08-10 | GSE37301 | GEO

Comparison of IL10-eGFP+ cells with IL10-eGFP- CD4+ T cells induced by in vivo immunisation

Project description:Here we perform QuantSeq 3' mRNA sequencing of RNA extracted from flow sorted splenic CD4+ Il10-eGFP+ or CD4+Il10eGFP- T cells from Tg4 Nr4a3-Tocky Il10-eGFP mice 24 hours after immunisation with 4 mg/kg of [4Y]-MBP. Our aim was to confirm the Tr1 cell phenotype within the Il10-eGFP+ T cell subset

2024-12-09 | GSE283286 | GEO

Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

Project description:We used a RAG2-GFP reporter mouse to show that RAG+ B lineage cells can be found in the small intestinal lamina proria in normally-housed mice at weaning age. We used microarry expression analysis to compare the RAG2+ population in the gut to the RAG2+ B lineage population in the bone marrow. Microarray was used to compare RAG2+ lamina propria B cells to RAG2+ bone marrow B cells.

2013-07-12 | GSE48805 | GEO

Unstable Foxp3+ regulatory T cells and altered antigen-presenting cells are associated with lipopolysaccharide-induced fetal loss in pregnant IL10 deficient mice

Project description:Maternal IL10 deficiency elevates susceptibility to fetal loss induced by the model Toll-like receptor agonist lipopolysaccharide, but the mechanisms are not well elucidated. Here we show that Il10 null mutant (Il10-/-) mice exhibit altered local T cell responses in pregnancy, exhibiting pronounced hyperplasia in para-aortic lymph nodes draining the uterus with >6-fold increased CD4+ and CD8+ T cells compared with wild-type controls. Amongst these CD4+ cells, Foxp3+ Treg cells were substantially enriched, with 11-fold higher numbers at day 9.5 post coitum (pc). Lymph node hypertrophy in Il10-/- mice was associated with more activated phenotypes in dendritic cells and macrophages, with elevated expression of MHCII, scavenger receptor and CD80. Affymetrix microarray revealed an altered transcriptional profile in Treg cells from pregnant Il10-/- mice, with elevated expression of Ctse (cathepsin E), Il1r1, Il12rb2 and Ifng. In vitro, Il10-/- Treg cells showed reduced steady state Foxp3 expression, and polyclonal stimulation caused greater loss of Foxp3 and reduced capacity to suppress IL17 in CD4+Foxp3- T cells. We conclude that despite a substantially expanded Treg cell pool, diminished stability of Treg cells, increased numbers of effector T cells, and altered phenotypes in dendritic cells and macrophages in pregnancy all potentially confer vulnerability to inflammation-induced fetal loss in Il10-/- mice. These findings suggest a pivotal role for IL10 in facilitating robust immune protection of the fetus from inflammatory challenge and suggest IL10 deficiency could contribute to human gestational disorders where altered T cell responses are implicated.

2015-07-30 | GSE71494 | 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