Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lipid-associated macrophages control metabolic homeostasis in a Trem2-dependent manner

ABSTRACT: Lipid-associated macrophages control metabolic homeostasis in a Trem2-dependent manner

PROVIDER: PRJNA527979 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8750230.fastq.gz	Fastqsanger.gz
	SRR8750240.fastq.gz	Fastqsanger.gz
	SRR8750250.fastq.gz	Fastqsanger.gz
	SRR8750260.fastq.gz	Fastqsanger.gz
	SRR8750270.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 150

Similar Datasets

Lipid-associated macrophages control metabolic homeostasis in a Trem2-dependent manner

Project description:Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream LAM molecular program during obesity, leading to adipocyte hypertrophy and both tissue-level and systemic hypercholesterolemia and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

2019-06-27 | GSE128518 | GEO

Lipid-Associated Macrophages Control Metabolic Homeostasis in a Trem2-Dependent Manner.

Project description:Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown. Using index and transcriptional single-cell sorting, we comprehensively map all adipose tissue immune populations in both mice and humans during obesity. We describe a novel and conserved Trem2+ lipid-associated macrophage (LAM) subset and identify markers, spatial localization, origin, and functional pathways associated with these cells. Genetic ablation of Trem2 in mice globally inhibits the downstream molecular LAM program, leading to adipocyte hypertrophy as well as systemic hypercholesterolemia, body fat accumulation, and glucose intolerance. These findings identify Trem2 signaling as a major pathway by which macrophages respond to loss of tissue-level lipid homeostasis, highlighting Trem2 as a key sensor of metabolic pathologies across multiple tissues and a potential therapeutic target in metabolic diseases.

| S-EPMC7068689 | biostudies-literature

Lipid Associated Macrophages' Promotion of Fibrosis Resolution during MASH regression requires TREM2

Project description:While macrophage heterogeneity during Metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood. Comparing macrophage heterogeneity during MASH progression vs regression, we identified specific macrophage sub- populations that are critical for MASH/fibrosis resolution. We elucidated the restorative pathways and gene signatures that define regression associated macrophages (RAM) and establish the importance of TREM2+ macrophages during MASH regression. Liver resident Kupffer cells are lost during MASH and are replaced by four distinct monocyte derived macrophage sub-populations. Trem2 is expressed in two macrophage sub- populations: (i) monocyte-derived macrophages occupying the Kupffer cell niche (MoKC) and (ii) lipid-associated macrophages (LAM). In regression livers, no new transcriptionally distinct MF sub-population emerged. However, the relative macrophage composition changed during regression compared to MASH. While MoKC was the major macrophage sub-population during MASH, they decreased during regression. LAM was the dominant macrophage sub-type during MASH regression and maintained Trem2 expression. Both MoKC and LAM were enriched in disease resolving pathways. Absence of TREM2 restricted the emergence of LAMs and formation of hepatic crown like structures (hCLS). TREM2+ macrophages are functionally important not only for restricting MASH-fibrosis progression, but also for effective regression of inflammation and fibrosis. TREM2+ MF are superior collagen degraders. Lack of TREM2+ macrophages also prevented elimination of hepatic steatosis and inactivation of HSC during regression, indicating their significance in metabolic co-ordination with other cell- types in the liver. TREM2 imparts this protective effect through multifactorial mechanisms, including improved phagocytosis, lipid-handling and collagen degradation.

2024-08-05 | GSE261829 | GEO

TREM2 regulates microglial lipid metabolism during aging in mice [RNA-Seq]

Project description:TREM2 is a microglial-specific gene implicated in late-onset Alzheimer's Disease (AD). Recent studies have identified that Trem2-deficient mice exhibit transcriptional changes in microglial gene expression that minimize the upregulation of lipid metabolism and lysosomal genes in AD disease models. We detect similiarly attenuated expression of lipid metabolism genes in microglia isolated from brains of aged Trem2 knockout mice.

2019-12-21 | GSE134031 | GEO

Expression data from wild type (WT) and TREM2 null alveolar macrophages (AM)

Project description:TREM-2 has been described to be a phagocytic receptor. We assessed the influence of TREM-2 on gene expression in alveolar macrophages (AM) In this data-set we characterised the differences in basal gene expression using affymetrix mouse 1.0 ST arrays between WT and TREM2-/- AM and observed TREM2 -/- AM to exhibt higher expression of opsonins 4 samples were analysed in biological duplicate (2 x WT and 2 x TREM2-/-)

2015-01-01 | E-GEOD-51378 | biostudies-arrayexpress

PLCG2 Regulates Divergent Microglial Functions via TREM2-Dependent and -Independent Signaling

Project description:We use genetically engineered human iPSC-derived microglia-like cells (iMG) to show that TREM2 signals through PLCγ2 to mediate cell survival, phagocytosis, and lipid metabolism following myelin challenge. Loss of TREM2 or PLCγ2 signaling leads to a shared signature of transcriptional dysregulation that underlies these phenotypes. However, PLCγ2 also signals downstream of Toll-like receptors to mediate inflammatory responses in a TREM2-independent manner. Therefore, PLCγ2 activity regulates divergent microglial functions via distinct TREM2-dependent and -independent signaling and may be involved in the transition to a microglial state associated with neurodegenerative disease.

2020-05-24 | GSE144120 | GEO

Lipid Associated Macrophages' Promotion of Fibrosis Resolution during MASH regression requires TREM2

Project description:Lipid Associated Macrophages' Promotion of Fibrosis Resolution during MASH regression requires TREM2

| PRJNA1089178 | ENA

Trem2 Promotes Foamy Macrophage Lipid Uptake and Survival in Atherosclerosis

Project description:To investigate the function of Trem2 on foamy macrophage gene regulation, we generated Trem2 deficientBV2 cells using CRISPR and comparedgene expression to Trem2 sufficientcontrols in the presence or absence of cholesterol loading.

2023-05-08 | GSE231659 | GEO

Trem2 Promotes Foamy Macrophage Lipid Uptake and Survival in Atherosclerosis

Project description:Trem2 Promotes Foamy Macrophage Lipid Uptake and Survival in Atherosclerosis

| PRJNA967260 | ENA

Lipid-anchored Proteasomes Control Membrane Protein Homeostasis

Project description:Lipid-anchored Proteasomes Control Membrane Protein Homeostasis

| PRJNA971586 | ENA