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RNA-seq of human adipose tissue macrophage subtypes in obesity

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189849 | GEO | 2022/01/31

REPOSITORIES: GEO

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Adipose tissue stromal cells from lean, obese, and formerly obese mice

Project description:Adipose tissue stromal cells contribute to the regulation of adipose tissue in lean and obese states. Myeloid cells such as adipose tissue macrophages (ATMs) and dendritic cells (ATDCs) undergo both quantitative and qualitative changes with obesity. Due to similarity in markers the identify of adipose tissue dendritic cells and macrophages has been elusive. We have refined prior protocols to unambiguously discern ATM and ATDC in mice. We used microarrays to compare the profiles of ATMs and ATDC from gonadal adipose tissue from lean, obese, and formerly obese mice. We also isolated preadipocytes (PA) from lean and obese mice for comparison. Male C57Bl/6 mice were fed normal diet (ND) or high fat diet (HFD) for 16 weeks. Weight loss (WL) mice were switched from the HFD to ND for 8 weeks. RNA was purified from FACS sorted cell populations (live cells only) obtained from gonadal/epididymal adipose tissue depots. ATMs were defined as CD11c+ (CD45+CD64+ CD11c+) or CD11c- (CD45+CD64+ CD11c-) ATMs. ATDC were defined as CD64- CD11c+. PA were defined as CD31- CD45- Sca1+ PDGFRA+.

2016-09-01 | GSE85846 | GEO

Differential lipid partitioning between adipocytes and tissue macrophages modulates macrophage lipotoxicity and M2/M1 polarization in obese mice.

Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points

2012-03-22 | E-GEOD-36669 | biostudies-arrayexpress

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Distinct macrophage populations upon physiological changes in adipose tissue [RNA-seq]

2018-06-04 | GSE113594 | GEO

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2020-05-22 | GSE151016 | GEO

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2010-12-07 | GSE24883 | GEO

Single-cell RNA-sequencing of stromal vascular cells (SVCs) from the epididymal fat of obese mice.

Project description:The obesity epidemic continues to worsen worldwide, driving metabolic and chronic inflammatory diseases. Thiazolidinediones (TZDs), such as rosiglitazone (Rosi), are PPARy ligands that promote anti-inflammatory changes in adipose tissue macrophages (ATMs) and cause insulin sensitization. We performed single-cell RNA-seuqnecing (scRNA-seq) to analyze the diversity and the phenotype of ATM subpopulations under Rosi and ATM-Exosome treatment.

2024-02-27 | GSE234046 | GEO

Single-cell transcriptome of stromal vascular fraction isolated from adipose tissue of lean and obese mice

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