Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses

ABSTRACT: Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses

PROVIDER: PRJNA795147 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses I

Project description:Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses I

| PRJNA792814 | ENA

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses II

Project description:Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses II

| PRJNA795149 | ENA

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses I

Project description:Macrophages are critical components of atherosclerotic lesions and their pro- and anti-inflammatory responses influence atherogenesis. Type-I interferons (IFNs) are cytokines that play an essential role in antiviral responses and inflammatory activation and have been shown to promote atherosclerosis. Although the impact of type-I IFNs on macrophage foam cell formation is well-documented, the effect of lipid accumulation in monocytes and macrophages on type-I IFN responses remains unknown. Here we examined IFN stimulated (ISG) and non-ISG inflammatory gene expression in mouse and human macrophages that were loaded with acetylated LDL (acLDL), as a model for foam cell formation. We found that acLDL loading in mouse and human macrophages specifically suppressed expression of ISGs and IFN-β secretion, but not other pro-inflammatory genes. The downregulation of ISGs could be rescued by exogenous IFN-β supplementation. Activation of the cholesterol-sensing nuclear liver X receptor (LXR) recapitulated the cholesterol-initiated type-I IFN suppression. Additional analyses of murine in vitro and in vivo generated foam cells confirmed the suppressed IFN signalling pathways and suggest that this phenotype is mediated via downregulation of interferon regulatory factor binding at gene promoters. Finally, RNA-seq analysis of monocytes of familial hypercholesterolemia (FH) patients also showed type-I IFN suppression which was restored by lipid-lowering therapy and not present in monocytes of healthy donors. Taken together, we define type-I IFN suppression as an athero-protective characteristic of foamy macrophages. These data provide new insights into the mechanisms that control inflammatory responses in hyperlipidaemic settings and can support future therapeutic approaches focusing on reprogramming of macrophages to reduce atherosclerotic plaque progression and improve stability.

2022-02-10 | GSE192709 | GEO

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses [RNA-seq]

Project description:Macrophages are critical components of atherosclerotic lesions and their pro- and anti-inflammatory responses influence atherogenesis. Type-I interferons (IFNs) are cytokines that play an essential role in antiviral responses and inflammatory activation and have been shown to promote atherosclerosis. Although the impact of type-I IFNs on macrophage foam cell formation is well-documented, the effect of lipid accumulation in monocytes and macrophages on type-I IFN responses remains unknown. Here we examined IFN stimulated (ISG) and non-ISG inflammatory gene expression in mouse and human macrophages that were loaded with acetylated LDL (acLDL), as a model for foam cell formation. We found that acLDL loading in mouse and human macrophages specifically suppressed expression of ISGs and IFN-β secretion, but not other pro-inflammatory genes. The down regulation of ISGs could be rescued by exogenous IFN-β supplementation. Activation of the cholesterol-sensing nuclear liver X receptor (LXR) recapitulated the cholesterol-initiated type-I IFN suppression. Additional analyses of murine in vitro and in vivo generated foam cells confirmed the suppressed IFN signaling pathways and suggest that this phenotype is mediated via down regulation of interferon regulatory factor binding at gene promoters. Finally, RNA-seq analysis of monocytes of familial hypercholesterolemia (FH) patients also showed type-I IFN suppression which was restored by lipid-lowering therapy and not present in monocytes of healthy donors. Taken together, we define type-I IFN suppression as an athero-protective characteristic of foamy macrophages. These data provide new insights into the mechanisms that control inflammatory responses in hyperlipidaemic settings and can support future therapeutic approaches focusing on reprogramming of macrophages to reduce atherosclerotic plaque progression and improve stability.

2022-07-01 | GSE193118 | GEO

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses

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

2022-02-10 | GSE193152 | GEO

Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses

Project description:Macrophages are critical components of atherosclerotic lesions and their pro- and anti-inflammatory responses influence atherogenesis. Type-I interferons (IFNs) are cytokines that play an essential role in antiviral responses and inflammatory activation and have been shown to promote atherosclerosis. Although the impact of type-I IFNs on macrophage foam cell formation is well-documented, the effect of lipid accumulation in monocytes and macrophages on type-I IFN responses remains unknown. Here we examined IFN stimulated (ISG) and non-ISG inflammatory gene expression in mouse and human macrophages that were loaded with acetylated LDL (acLDL), as a model for foam cell formation. We found that acLDL loading in mouse and human macrophages specifically suppressed expression of ISGs and IFN-ÃŽÂ² secretion, but not other pro-inflammatory genes. The downregulation of ISGs could be rescued by exogenous IFN-ÃŽÂ² supplementation. Activation of the cholesterol-sensing nuclear liver X receptor (LXR) recapitulated the cholesterol-initiated type-I IFN suppression. Additional analyses of murine in vitro and in vivo generated foam cells confirmed the suppressed IFN signalling pathways and suggest that this phenotype is mediated via downregulation of interferon regulatory factor binding at gene promoters. Finally, RNA-seq analysis of monocytes of familial hypercholesterolemia (FH) patients also showed type-I IFN suppression which was restored by lipid-lowering therapy and not present in monocytes of healthy donors. Taken together, we define type-I IFN suppression as an athero-protective characteristic of foamy macrophages. These data provide new insights into the mechanisms that control inflammatory responses in hyperlipidaemic settings and can support future therapeutic approaches focusing on reprogramming of macrophages to reduce atherosclerotic plaque progression and improve stability.

| EGAS00001005955 | EGA

Data Access Commitee - Monocyte and macrophage lipid accumulation results in downregulated type-I interferon responses - FH monocytes RNA sequencing data

Project description:Data Access Committee EGAC00001002495

| EGAC00001002495 | EGA

Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

Project description:Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

| PRJNA723851 | ENA

5-hydroxymethylcytosine Accumulation in Postmitotic Neurons Results in Functional Demethylation of Expressed Genes

Project description:5-hydroxymethylcytosine Accumulation in Postmitotic Neurons Results in Functional Demethylation of Expressed Genes

| PRJNA377722 | ENA

Functional evaluation of neutrophil of patients at high risk for infection treated with monocyte/ neutrophil apheresis

Project description:Interventions: monocyte/neutrophil apheresis non monocyte/neutrophil apheresis Primary outcome(s): Evaluation neutrophil function of patients at high risk for postoperative infection treated with monocyte/neutrophil apheresis Study Design: Parallel Non-randomized

| 2627605 | ecrin-mdr-crc

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