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The impact of Srebf2 deletion on the transcriptional phenotype of visceral adipose tissue (VAT) regulatory T (Treg) cells

ABSTRACT: The impact of Srebf2 deletion on the transcriptional phenotype of visceral adipose tissue (VAT) regulatory T (Treg) cells

PROVIDER: PRJNA1015733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26045806_1.fastq.gz	Fastqsanger.gz
	SRR26045806_2.fastq.gz	Fastqsanger.gz
	SRR26045807_1.fastq.gz	Fastqsanger.gz
	SRR26045807_2.fastq.gz	Fastqsanger.gz
	SRR26045808_1.fastq.gz	Fastqsanger.gz

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The impact of Srebf2 deletion on the transcriptional phenotype of visceral adipose tissue (VAT) regulatory T (Treg) cells

Project description:Regulatory T (Treg) cells are highly enriched in the visceral adipose tissue (VAT) to maintain metabolic homeostasis, but they are lost during obesity. VAT Treg cells exhibit enhanced Srebf2-dependent cholesterol metabolism compared lymphoid tissue Tregs at steady state, but this metabolic pathway is disrupted during obesity. Therefore, the goal of this study is to determine the impact of Treg-specific Srebf2 deletion on the transcriptional phenotype of bulk Foxp3+ VAT or splenic Tregs.

2025-01-10 | GSE243021 | GEO

Obesity disrupts cellular cholesterol homeostasis to inhibit the homeostatic clonal expansion of ST2hi VAT Treg cells

Project description:Regulatory T (Treg) cells are highly enriched in the visceral adipose tissue (VAT) to maintain metabolic homeostasis, but they are lost during obesity. Currently, how VAT Treg cells rewire cellular metabolism to support their homeostatic clonal expansion, and whether this process is disrupted in obesity, is unclear. Here, we found that cholesterol metabolism was uniquely upregulated in VAT-, but not other non-lymphoid-tissue Treg cells. Disrupting cholesterol homeostasis (CH) by Treg-specific deletion of Srebf2 led to a specific loss of VAT Treg cells and enhanced obesity-induced systemic metabolic dysfunction. Mechanistically, Srebf2-mediated CH potentiated strong TCR signaling, which specifically promoted the clonal expansion of ST2hi, but not other, VAT Treg subsets. However, long-term high-fat-diet feeding disrupted VAT Treg CH and impaired ST2hi VAT Treg clonal expansion. Restoring Treg CH rescued VAT Treg accumulation in obese mice, suggesting CH modulation could be a potential option for Treg-targeted therapies in obesity-associated metabolic diseases.

2025-01-10 | GSE243563 | GEO

The impact of IL-33 on Srebf2-dependent cholesterol gene expression in ST2+ eVAT Tregs

Project description:Tregs are highly enriched in the eVAT of male mice. We show that ST2+ VAT Tregs preferentially upregulate and depend on Srebf2-mediated cholesterol metabolism compared their spleen Treg or ST2- VAT Treg counterparts. However, it is unclear whether this increased reliance on cholesterol metabolism is a consequence elevated IL-33 signaling in ST2+ Tregs. Therefore, the goal of experiment is to determine whether IL-33 signaling influences Srebf2-dependent cholesterol gene expression in ST2+ eVAT Tregs in vivo.

2025-01-10 | GSE272435 | GEO

Gene expression of visceral adipose regulatory T cells from mice with specific deletion of insulin receptor in the cells

Project description:Visceral adipose tissue (VAT) regulatory T cells (Tregs) control inflammation and metabolism. Diet-induced obesity causes hyperinsulinemia and diminishes VAT Treg number and function, but whether these two phenomena were mechanistically linked was unknown. We hypothesized that excessive insulin signaling in obesity negatively impact VAT Tregs. Using Treg-specific insulin receptor deletion (Foxp3-cre;Insr-fl/fl) mice, we compared the gene expression of VAT Tregs from control and knockout mice in obesity and aging, two models of hyperinsulinemia. We found that genes associated with Treg functions were altered in Tregs lacking insulin receptor.

2020-05-22 | GSE151016 | GEO

Transcriptional profiling of Regulatory T (Treg) cells in obesity

Project description:We reported transcriptional characterization of vTreg53 TCR transgenic Treg cells from splenic and visceral adipose tissue (VAT) in mice fed with normal chow diet (NCD) or high fat diet (HFD) for different durations. We also reported transcriptional profile of VAT Treg cells stimulated by IFNa in vitro. Through this analysis, we found that the reduction of VAT Treg cells during obesity is driven by increased production of IFNa in VAT.

2021-05-20 | GSE174706 | GEO

Transcriptional characterization of visceral adipose tissue (VAT) mesenchymal stromal cell (mSC) subtypes in male and female C57BL/6 mice.

Project description:Regulatory T cells (Tregs) are key brakes on the VAT inflammation that regulates local and systemic metabolic tenor. The cytokine, IL-33, expands and sustains the unique Treg population residing within VAT. Making use of single-cell RNA sequencing, we identified the major IL-33 producers in VAT to be particular mSC subtypes, related to but distinct from adipocyte progenitor cells. We further characterize these subsets by individually isolating them and performing bulk-RNA sequencing. We explored modulation of the VAT-mSC (VmSC) landscape with physiologic variables such as age and sex, as well as pathogenic states like obesity. We uncovered a VAT Treg:stromal-cell negative regulatory loop that keeps the potent effect of IL-33 under rein.

2019-02-22 | GSE126891 | GEO

Transcriptional profiling of vTreg53 TCR transgenic Regulatory T (Treg) cells stimulated by agonist peptide

Project description:We reported transcriptional characterization of vTreg53 TCR transgenic Treg cells from splenic/lymph nodes and visceral adipose tissue (VAT) stimulated by agonsit peptide fat1562. We identified that peptide immunization is associated with TCR activation and that the VAT Treg transcriptome is largely maintained in the presence of antigen stimulation

2020-08-01 | GSE150173 | GEO

Transcriptional profiling of Regulatory T (Treg) cells and CD4+ conventional T (Tconv) cells from vTreg53 TCR transgenic and PPARg reporter mice

Project description:We reported transcriptional characterization of Treg and Tconv cells from thymic, splenic, and visceral adipose tissue (VAT) of vTreg53 TCR transgenic mice and control littermates. We examined the effect of Foxp3 on splenic and VAT CD4+ T cell transcriptome. We profiled gene expression in a novel PPARg+ splenic Treg population. We uncovered that the characteristic phenotype of VAT Treg cells was acquired in two stages.

2018-06-08 | GSE113393 | GEO

Metabolic control in VAT by Tregs through OSM-mediated suppression of adipogenesis

Project description:Regulatory T cells (Tregs) play diverse roles in tissue homeostasis. In visceral adipose tissue (VAT), resident Tregs, enriched with PPARγ, are clonally expanded in a IL-33 dependent manner. However, the tissue-specific functions of VAT Tregs, with unique transcriptome compared to spleen or other peripheral tissues, remain largely unknown. We identified two PPARγ+ mesenchymal stromal cells in VAT (VmSCs), named VmSC4s (PPARγ+Thy1-) and 5s (PPARγ+Thy1+). Lineage-tracing and transcriptome analysis revealled that VmSC4s contain precursors for VmSC5s. We also demonstrated that VAT Tregs directly suppress adipogenic differentation of VmSC5s through Oncostain M (OSM) to promote insulin sensitivity and glucose tolerance. Thus, VAT-Treg-derived OSM and VmSCs-displayed OSMR maintain tissue homeostasis via limiting the differentiation of dysfunctional adipocytes, which provide therapeutic targets for treating obesity and diabetes.

2023-08-01 | GSE226889 | GEO

Inflammation-dependent differentiation of two distinct regulatory T cell populations in the visceral adipose tissue shapes systemic metabolism [RNA-seq III]

Project description:Visceral adipose tissue (VAT) is an endocrine organ critical for energy storage and metabolic homeostasis. Its function, at least in part, is controlled by immune cells, including Foxp3+ regulatory T (Treg) cells, which restrain VAT inflammation and glucose intolerance. Here we uncover that the VAT harbours two distinct Treg cell populations, prototypical ST2+ Treg cells, that are enriched in males and depend on the cytokine IL-33 and the transcription factor PPAR and a previously uncharacterized population of VAT Treg cells that express the chemokine receptor CXCR3+, are enriched in females and depend on the transcription factor T-bet. We further show that the transcription factor GATA3 promoted differentiation of ST2+ VAT Treg cells and together with PPAR and IL-33 repressed the differentiation of CXCR3+ Treg cells. CXCR3+ VAT Treg cells developed from naïve Treg cells in a cytokine IFN- dependent manner. Finally, we demonstrate that ST2+ Treg cells promoted glucose tolerance, while CXCR3+ Treg cells limited VAT inflammation in a sex specific manner. This study for the first time establishes how inflammation determines the developmental trajectories of two functionally and molecularly distinct Treg cell types in the VAT.

2024-03-22 | GSE237835 | GEO

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