Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Utilizing ex vivo generated double negative T cells prevents the development and progression of nonalcoholic steatohepatitis

ABSTRACT: Utilizing ex vivo generated double negative T cells prevents the development and progression of nonalcoholic steatohepatitis

PROVIDER: PRJNA554829 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9693260.fastq.gz	Fastqsanger.gz
	SRR9693261.fastq.gz	Fastqsanger.gz
	SRR9693262.fastq.gz	Fastqsanger.gz
	SRR9693263.fastq.gz	Fastqsanger.gz
	SRR9693258.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Nonalcoholic steatohepatitis in adolescents undergoing bariatric surgery

Project description:The genomic landscape of hepatic tissue affected by nonalcoholic steatohepatitis (NASH) in severely obese adolescents undergoing bariatric surgery is unknown. Our purpose here was to uncover genomic profiles of obese controls, and obese cases with nonalcoholic fatty liver disease (NAFLD), borderline nonalcoholic steatohepatitis, and definite nonalcoholic steatohepatitis, in order to clarify molecular functions, biological processes, and pathways that are dysregulated in nonalcoholic steatohepatitis in the severely obese adolescent. In a prospective observational cohort study, we have intra-operatively obtained 165 liver samples; of these 67 were submited for microarray analysis. Through ANOVA, we found 8648 genes with differential regulation between the four histologies; from these, we uncovered gene signatures shared between borderline and definite nonalcoholic steatohepatitis, and gene sets with differential effects between borderline and definite.

2017-07-21 | GSE66676 | GEO

Myeloid FoxO1 in Nonalcoholic Steatohepatitis

Project description:Myeloid FoxO1 in Nonalcoholic Steatohepatitis

| PRJNA839093 | ENA

Utilizing ex vivo generated double negative T cells prevents the development and progression of nonalcoholic steatohepatitis

Project description:Methods: The DNT cells incubation with CD3/CD28 antibodies were stimulated with IL-10 (50 ng/ml) for 24 hours, then transcriptome sequencing studies were performed on DNT cells RNA. Results: The distributions of up- (107) and downregulated (114) genes (≥ 1.5-fold difference, padj < 0.05) compared with without IL-10-treated DNT were depicted in a volcano plot. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed that changed genes from IL-10-stimulated monocytes were involved in the immune response; inflammatory response; regulation of apoptotic and proliferation; cytolysis; cytokine-cytokine receptor interaction; and T cell receptor signaling pathway, among others. Compared with control DNT cells, IL-10-treated DNT exhibited downregulated levels of cell survival and activation genes (Bcl-xl, Cytc, Epcam, and Spi1), cell cytotoxicity genes (Nkp46, Klrg1, Slamf6, Cd107a, Cd161, and Cd226), immune responses genes (Lta, Cd127, H2-Oa, and H2-Dma), and upregulated cell exhaustion genes (Pd-1, Ctla4, and Tim3).In this study, we found IL-10 stimulated DNT cells highly expressed PI3K-AKT signaling genes, such as Jak3, Pik3ap1, Pik3cb, and Sgk1, and MAPK pathway genes, such as Stmn1, Fos, Kras, Nras, and Map3k5, which indicated that IL-10 upregulated NKG2A expression in DNT cells may through these pathways.

2020-11-11 | GSE134346 | GEO

AGXT overexpression during nonalcoholic steatohepatitis in mice

Project description:To investigate the effects of AAV8-mediated overexpression of AGXT in mice with diet-induced nonalcoholic steatohepatitis compared to AAV8-GFP

2023-02-19 | GSE224097 | GEO

Nonalcoholic fatty liver, but not nonalcoholic steatohepatitis is a protective factor to tetrachloroethylene-associated kidney effects in male C57BL/6J mice

Project description:Purpose: We investigated the tetrachloroethylene associated changes in kidney transcriptomes among healthy mice, nonalcoholic fatty liver disease mice, and nonalcoholic steatohepatitis mice.

2019-02-13 | GSE115641 | GEO

AGXT overexpression during nonalcoholic steatohepatitis in mice

Project description:AGXT overexpression during nonalcoholic steatohepatitis in mice

| PRJNA929896 | ENA

Hepatic microRNA signatures in experimental nonalcoholic steatohepatitis

Project description:Hepatic microRNA signatures in experimental nonalcoholic steatohepatitis

| PRJNA557444 | ENA

Neutralization of Oxidized Phospholipids Restrains Nonalcoholic Steatohepatitis

Project description:Neutralization of Oxidized Phospholipids Restrains Nonalcoholic Steatohepatitis

| PRJNA575823 | ENA

Tranilast inhibits hepatic lipid response in nonalcoholic steatohepatitis by deacetylating LKB1

Project description:Nonalcoholic fatty liver disease (NAFLD), a progressive hepatic disease with ectopic fat accumulation, can evolve toward nonalcoholic steatohepatitis (NASH). To date, there is still no approved drug therapy, which remains a major unmet need. Previous study has indicated that tranilast ameliorates hepatic fibrosis and stellate cells activation in dietary rat model of NASH. However, the precise mechanism of tranilast in anti-NASH remains unclear.

2025-02-19 | GSE249350 | GEO

Myeloid FoxO1 in Nonalcoholic Steatohepatitis

Project description:Our objective is to determine the role of myeloid FoxO1 in regulating hepatic lipid metabolism and its contribution to nonalcoholic steatohepatitis (NASH) in mice. We generated mice with conditional FoxO1 depletion in myeloid cells, using the FoxO1-LoxP/LysM-Cre system. We then fed myeloid cell-conditional FoxO1-knockout and wild-type male mice a NASH-inducing diet for 25 weeks. Then mice in both groups were euthanized and the liver tissues were procured for the preparation of total RNAs, which were subjected to RNA-seq assay. While myeloid FoxO1 was upregulated in animal models and human subjects with NASH, the underlying mechanism is poorly understood. We found that myeloid cell conditional FoxO1-knockout mice were protected from developing NASH, culminating in the reduction of hepatic inflammation, steatosis and fibrosis. Mechanistically, FoxO1 counteracts Stat6 to skew macrophage polarization from M2 toward M1 signatures to perpetuate hepatic inflammation in NASH. FoxO1 appears as a pivotal mediator of macrophage activation in response to overnutrition and a therapeutic target for ameliorating hepatic inflammation to stem the disease progression from benign steatosis to NASH.

2022-05-24 | GSE203227 | 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