Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

ABSTRACT: High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

PROVIDER: PRJNA1243316 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32907123_1.fastq.gz	Fastqsanger.gz
	SRR32907123_2.fastq.gz	Fastqsanger.gz
	SRR32907124_1.fastq.gz	Fastqsanger.gz
	SRR32907124_2.fastq.gz	Fastqsanger.gz
	SRR32907125_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [liver]

Project description:The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined liver transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

2025-04-04 | GSE293183 | GEO

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:The goal of this project is to investigate the mechanisms through which high fat diet (HFD) exacerbates colitis via the liver-gut axis, particularly focusing on liver dysregulated lipid metabolism and intestinal autophagy. We examined colon transcriptomes of C57BL6/J mice fed a control diet (CD) or HFD with or without dextran sulfate sodium (DSS) by RNA seq analysis.

2025-07-02 | GSE293222 | GEO

High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

Project description:High-Fat Diet-Induced Liver-Gut Crosstalk Suppresses Autophagy and Exacerbates Colitis [colon]

| PRJNA1243378 | ENA

ITIH5-mediated fibroblast/macrophage crosstalk exacerbates cardiac remodelling after myocardial infarction

Project description:ITIH5-mediated fibroblast/macrophage crosstalk exacerbates cardiac remodelling after myocardial infarction

| PRJNA1140853 | ENA

Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

Project description:Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

| PRJNA1063625 | ENA

BMP9 and BMP10 coordinate liver cellular crosstalk to maintain liver health

Project description:BMP9 and BMP10 coordinate liver cellular crosstalk to maintain liver health

| PRJNA1023032 | ENA

Placental-Liver Crosstalk in the Control of Pregnancy

Project description:Placental-Liver Crosstalk in the Control of Pregnancy

| PRJEB50835 | ENA

Gene regulation in autophagy and apoptosis juncture

Project description:Autophagy to apoptosis switching event is an unexplored area. We were interested to explore the gene expression profile at this juncture. Our Microarray data emphasized that among all eNOS and p62 genes were markedly induced. In fuctional level eNOS expression activates mTORC1 followed by inhibition of autophagy. This ultimately allowed accumulation of p62 . Intraccellular accumulation of p62 sequestered unfolded toxic protein aggregates in mitochondria and ER resulting in to impaired redox regulation. Intraccelular ROS generation further sensitized cells for apoptosis and tilted autophagic response to apoptosis. Cells were treated with Tunicamycin as an inducer of both autophagy and apoptosis. At early stage of Tunicamycin treatment 24h , prostate cancer cell PC3 showed activation of autophagic process where apoptosis was not evident. Sustained ER stress with Tunicamycin induced late apoptoisis at 72h of treatment. Hence we isolated total RNA from Untreated cells, cells with Tunicamycin treatment after 24h and 72h. Further the RNA were used to perform whole genome microarray to analyze the gene expression profile at autophagy and apoptosis juncture. The selected genes were also validated by qPCR and western bot. Morover RNAi study were implemented to evaluate the signaling crosstalk at the juncture of autophagy and apoptosis.

2014-05-22 | E-GEOD-38643 | biostudies-arrayexpress

Project description:Autophagy related 14 regulates liver homeostasis and function

| PRJNA1258151 | ENA

Defective autophagy in CD4 T cells drives liver fibrosis via type 3 inflammation

Project description:Abstract: Conventional CD4 T cells represent a major source of inflammatory mediators that drive progression of chronic liver disease to fibrosis and to end-stage cirrhosis. Identification of T cell pathways that limits the inflammatory response could thus have therapeutic relevance. Here we show, using both human samples and mouse models, that autophagy is deficient in CD4 T cells from patients with advanced fibrosis, and that loss of autophagy following genomic deletion of ATG5 in T cells is associated with the emergence of pathogenic IL-17A+IFN-g+ Th17 T cells that drive liver fibrosis in mice. Mechanistically, liver CD4 T cells lacking autophagy display a Th17 glycolytic phenotype associated with enhanced type 3 cytokine (i.e. IL-17A and GM-CSF) release, shifting hepatic myofibroblasts, hepatocytes and macrophages toward a proinflammatory phenotype. We also show that autophagy can be rescued in CD4 T cells from patients with extensive liver fibrosis, leading to decreased frequency of pathogenic Th17 cells and reduced GM-CSF levels; in addition, limited fibrosis is observed in mice in which Rubicon, a negative regulator of autophagy, is deleted specifically in their T cells. Our findings thus implicate autophagy in CD4 T cells as a key therapeutic target to control inflammation-driven fibrosis during chronic liver injury.

2025-04-14 | GSE292735 | 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