Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Macrophage heterogenity in liver and adipose during obesity

ABSTRACT: Liver and adipose tissue undergo dynamic inflammatory changes during the progression of obesity. This study was designed to evaluate the changes in gene expression profile and function of subpecific macophage subsets.

ORGANISM(S): Mus musculus

PROVIDER: GSE163003 | GEO | 2020/12/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Macrophage heterogenity in liver and adipose during obesity

Project description:Macrophage heterogenity in liver and adipose during obesity

| PRJNA684317 | ENA

Adipose Tissue Macrophage Accrual in Obesity

Project description:Adipose Tissue Macrophage Accrual in Obesity

| PRJNA634570 | ENA

Perivascular Mesenchymal Cells Control Adipose Tissue Macrophage Accrual in Obesity

Project description:Chronic low-grade visceral white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a subpopulation of adipose tissue perivascular (PDGFRb+) cells, termed “fibro-inflammatory progenitors” (FIPs), activate pro-inflammatory signaling cascades shortly after the onset of high-fat diet feeding of mice and regulate pro-inflammatory macrophage accumulation in WAT in a TLR4-dependent manner. FIPs activation in obesity is mediated by the downregulation of ZFP423, identified here as a transcriptional co-regulator of NFkB. Biochemical analysis of ZFP423-protein complexes and ChIP-seq analysis reveal that ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NFkB by inducing a p300 to NuRD co-regulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRb+ cells suppresses inflammatory signaling in FIPs and attenuates metabolic inflammation of visceral WAT in obesity. Inducible inactivation of Zfp423 in PDGFRb+ cells increases FIP activity, exacerbates adipose macrophage accrual, and promotes WAT dysfunction. These studies implicate perivascular mesenchymal cells as important regulators of chronic adipose tissue inflammation in obesity and identify ZFP423 as a transcriptional break on NFkB signaling.

2020-09-01 | GSE151092 | GEO

Adipose Tissue Omics In Obesity

Project description:Adipose Tissue Omics In Obesity

| PRJNA1006463 | ENA

Adipose Tissue Omics In Obesity

Project description:Adipose Tissue Omics In Obesity

| PRJNA1006496 | ENA

Transcriptome profiling of omental adipose tissues in human obesity by RNA-Seq

Project description:Purpose: To profile the transcriptomes of omental adipose tissues from obese and lean humans. Methods: Omental adipose tissues from obese and lean patients were subjected to RNA-Seq. Results: Differential expression analysis identified 206 dysregulated genes (p-value < 0.05 by moderated t-test and fold change M-bM-^IM-% 2 in obesity) that are known to be involved in a multitude of functions, including response to stress, inflammatory response and leukocyte adhesion. Differential splicing analysis uncovered the possible role of TLR4 RNA splicing in obesity. Our findings suggest that, as a person experiences weight gain/obesity, the adipose splicing pattern of TLR4 transcripts changes in favor of activation of TLR4 signaling, which in turn may contribute to the progression of obesity-related inflammation and complications. Conclusion: This study provides a look into the transcriptome of disease-state adipose tissue in obesity, and demonstrates the potential importance of aberrant RNA splicing and expression in obesity-associated immune dysregulation. Study design is of cross-sectional nature. Seven samples (three obese and four lean) were analyzed.

2015-02-11 | E-GEOD-55008 | biostudies-arrayexpress

Visceral adipose tissue macrophage subsets

Project description:Visceral adipose tissue macrophage subsets

| PRJNA484897 | ENA

Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity

Project description:This SuperSeries is composed of the following subset Series: GSE25401: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [gene expression] GSE25470: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [miRNA data] GSE25910: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [differentiation data] Refer to individual Series

2012-08-12 | E-GEOD-25402 | biostudies-arrayexpress

Mural Cell ZFP423 Controls Adipose Tissue Macrophage Accrual in Obesity [ChIP-seq]

Project description:Chronic low-grade visceral white adipose tissue (WAT) inflammation is a hallmark of metabolic syndrome in obesity. Here, we demonstrate that a specific subpopulation of adipose tissue perivascular (PDGFRb+) stromal cells, termed “fibro-inflammatory progenitors” (FIPs), activate pro-inflammatory signaling cascades shortly after the onset of high-fat diet feeding of mice and control the accumulation of pro-inflammatory macrophages in WAT. The activation of FIPs is mediated by the downregulation of ZFP423, identified here as a transcriptional co-regulator of NFkB. Biochemical analysis of ZFP423-protein complexes and ChIP-seq analysis reveal that ZFP423 suppresses the DNA-binding capacity of the p65 subunit of NFkB by inducing a co-regulator switch. Doxycycline-inducible expression of Zfp423 in PDGFRb+ cells suppresses inflammatory signaling in FIPs and attenuates macrophage accumulation within visceral WAT of obese mice. Conversely, inducible inactivation of Zfp423 in PDGFRb+ cells increases FIP activity, exacerbates adipose macrophage accrual, and promotes WAT dysfunction in obese mice. These studies implicate mural cells as sentinels and gatekeepers of adipose tissue inflammation in obesity.

2020-09-01 | GSE134868 | GEO

RNA-seq of human adipose tissue macrophage subtypes in obesity

Project description:We profiled three prominent ATM subtypes from human visceral omental adipose tissue in obesity by RNA-seq. In the related manuscript, we evaluated differences in their signatures and their relationship to type 2 diabetes: Visceral (VAT) and subcutaneous (SAT) adipose tissue samples were collected from diabetic and non-diabetic obese subjects to evaluate cellular content and gene expression. VAT CD206+CD11c− ATMs were increased in diabetic subjects, scavenger receptor-rich with low intracellular lipids, secreted proinflammatory cytokines, and diverged significantly from two CD11c+ ATM subtypes, which were lipid-laden, lipid antigen presenting, and overlapped with monocyte signatures. Furthermore, diabetic VAT was enriched for CD206+CD11c− ATM and inflammatory signatures, scavenger receptors, and MHC II antigen presentation genes. VAT immunostaining found CD206+CD11c⁻ ATMs concentrated in vascularized lymphoid clusters adjacent to CD206⁻CD11c+ ATMs, while CD206+CD11c+ were distributed between adipocytes. Our results suggest ATM subtype-specific profiles that uniquely contribute to the phenotypic variation in obesity.

2022-01-31 | GSE189849 | 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