Similar Datasets
Project description:We profiled the transcriptome of sorted BAT and SAT Tregs and the transcriptional effects of BAT activating factors on whole-BAT transcriptomes when Tregs are present or absent.
2025-08-27 | GSE271779 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-08-27 | GSE272981 | GEO
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
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
Project description:Using RNA isolated from subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) samples obtained from control and class I, II and III obese patients undergoing inguinal hernia repair and laparoscopic cholecystectomy, we compared the gene expression profiles between SAT and VAT using microarrays and validated the findings by real-time quantitative PCR. Two-condition experiment, SAT vs. VAT tissue. Biological replicates: 8 SAT replicates, 8 VAT replicates.
2016-07-20 | E-GEOD-84599 | biostudies-arrayexpress
Project description:Regulatory T (Treg) cells located within parenchymal tissues safeguard tissue homeostasis. A paradigmatic "tissue-Treg" population is that found in visceral-adipose tissue (VAT) of male mice. VAT-Treg cells have a unique transcriptome, are clonally expanded, and promote metabolic health through effects on local immunocytes and adipocytes. Because of their rarity and inaccessibility, cardinal questions such as what factors control their accumulation in fat and when/where/how do they adopt their distinctive phenotype remained unanswered. We addressed these issues using VAT- Treg T-cell-receptor (TCR) transgenic mice. Accumulation of VAT-Tregs was driven by combined effects of TCR specificity, Foxp3 expression, and a cell-intrinsic response to interleukin-33. Their characteristic phenotype emerged in two stages: a minority of splenic Treg cells weakly up-regulated a slice of the VAT-Treg transcriptional signature, reflecting cell activation, but the definitive phenotype, arming cells for fat survival, was manifest only in VAT. This deeper understanding of tissue-Treg generation should facilitate precision-targeting strategies.
2018-06-08 | GSE113412 | GEO
Project description:The accumulation of visceral adipose tissue (VAT) is strongly associated with cardiovascular disease and diabetes. In contrast, individuals with increased subcutaneous adipose tissue (SAT) without corresponding increases in VAT are associated with a metabolic healthy obese phenotype. These observations implicate dysfunctional VAT as a driver of disease processes, warranting investigation into obesity-induced alterations of distinct adipose depots. To determine the effects of obesity on adipose gene expression, mice were fed either a high fat or normal laboratory diet for 12-14 months. Mesenteric VAT and hindlimb SAT were isolated from four lean controls and four obese mice for bulk RNA- sequencing. AT from lean controls served as a reference to obesity-induced changes. The long-term high fat diet induced the expression of 169 and 814 unique genes in SAT and VAT, respectively. SAT from obese mice exhibited a total of 308 differentially expressed genes (164 upregulated, 144 downregulated). VAT from obese mice exhibited 690 differentially expressed genes (262 genes upregulated, 428 downregulated). KEGG pathway and GO analyses revealed that metabolic pathways were upregulated in SAT vs. downregulated in VAT while inflammatory signaling was upregulated in VAT. We next determined common genes that were differentially regulated between SAT and VAT in response to obesity and identified four genes that exhibited this profile: elovl6 and kcnj15 were upregulated in SAT/downregulated in VAT while trdn and hspb7 were downregulated in SAT/ upregulated in VAT. We propose that these genes in particular should be further pursued to determine their roles in SAT vs. VAT with obesity.
2024-06-12 | GSE269663 | GEO
Project description:FA-SAT is a satellite DNA sequence present and transcribed in many Bilateria species, what may anticipate a conserved and significant function in these genomes. Here we prove that in cat and human cells, FA-SAT satellite transcripts play a nuclear function at the G1 phase of the cell cycle. We identified and demonstrated that the main FA-SAT non-coding RNA interactor is the PKM2 protein. Our work shows that the disruption of the FA-SAT ncRNA/PKM2 protein complex, by the depletion of either FA-SAT or PKM2, results in the same phenotype—apoptosis. Moreover, the ectopic overexpression of FA-SAT in tumour human cells did not affect the cell cycle progression. In sum, our data reveal a new player, FA-SAT RNA, a non-coding satellite RNA, which interacts with the PKM2 nuclear protein. This ribonucleoprotein is involved in apoptosis and cell cycle progression, what foresees a promising new target for studies in cancer processes that rely on these pathways.
2020-03-19 | PXD010081 | Pride
Project description:Cardiometabolic diseases are common in persons with HIV (PWH) on antiretroviral therapy (ART), which has been attributed to preferential lipid storage in visceral adipose tissue (VAT) compared with subcutaneous adipose tissue (SAT). However, the relationship of SAT-specific cellular and molecular programs with VAT volume is poorly understood in PWH. We characterized SAT cell-type specific composition and transcriptional programs that are associated with greater VAT volume in PWH on contemporary ART. We enrolled PWH on long-term ART with a spectrum of metabolic health.We enrolled PWH on long-term ART with a spectrum of metabolic health. Ninety-two participants underwent SAT biopsy for bulk RNA sequencing and 43 had single-cell RNA sequencing. Computed tomography quantified VAT volume and insulin resistance was calculated using HOMA2-IR. VAT volume was associated with HOMA2-IR (p<0.001). Higher proportions of SAT intermediate macrophages (IMs), myofibroblasts, and MYOC+ fibroblasts were associated with greater VAT volume using partial Spearman’s correlation adjusting for age, sex, and body mass index (r =0.34-0.49, p<0.05 for all). Whole SAT transcriptomics showed PWH with greater VAT volume have increased expression of extracellular matrix (ECM)- and inflammation-associated genes, and reduced expression of lipolysis- and fatty acid metabolism-associated genes. In PWH, greater VAT volume is associated with higher proportion of SAT IMs and fibroblasts, and a SAT ECM and inflammatory transcriptome, which is similar to findings in HIV-negative persons with obesity. These data identify SAT cell-type specific changes associated with VAT volume in PWH that could underlie the high rates of cardiometabolic diseases in PWH, though additional longitudinal studies are needed to define directionality and mechanisms.
2024-05-22 | GSE243957 | GEO
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