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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

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			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

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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.

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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.

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

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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

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RPA1 Remodels Liver Chromatin Architecture to Maintain Lipid Metabolic Homeostasis

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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

RPA1 Remodels Liver Chromatin Architecture to Maintain Lipid Metabolic Homeostasis

Project description:Replication protein A(RPA), a ssDNA binding protein complex, participates in DNA replication, recombination and damage repair, but its physiological function remains elusive. Here, we show that heterozygous Rpa1 knockout mice were developmentally normal, but hypersensitive to ageing and high-fat-diet (HFD) induced hepatic steatosis. Liver specific deletion of Rpa1 leads to impaired lipid beta-oxidation, hepatic steatosis and subsequently hepatocellular carcinoma (HCC). Assays for RNA-seq, pull-down and transposase-accessible chromatin sequencing (ATAC-seq) reveal that RPA1 is required for transcription of a subgroup of lipid metabolic genes via altering chromatin accessibility landscape. Thus, our results suggest that RPA1 is a critical regulator of gene transcription and chromatin remodeling, linking a guardian of genome stability to lipid metabolic homeostasis.

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