Prdm16 overexpression effect on inguinal white adipose tissue:stromal-vascular cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE129084 | GEO | 2019/07/31
REPOSITORIES: GEO
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Project description:Inguinal white adipose tissue (iWAT) is essential for the beneficial effects of exercise training on metabolic health. The underlying mechanisms for these effects are not fully understood and here, we test the hypothesis that exercise training results in a more favorable iWAT structural phenotype. Using biochemical, imaging, and multi-omics analyses we find that 11-days of wheel running in male mice causes profound iWAT remodeling including decreased extracellular matrix (ECM) deposition, increased vascularization and innervation. We identify adipose stem cells as one of the main contributors to training-induced ECM remodeling, show that the PRDM16 transcriptional complex is necessary for iWAT remodeling and beiging, and discover neuronal growth regulator 1 (NEGR1) as a link between PRDM16 and neuritogenesis. Moreover, we find that training causes a shift from hypertrophic to insulin-sensitive adipocyte subpopulations. Exercise training leads to remarkable adaptations to iWAT structure and cell-type composition that can confer beneficial changes in tissue metabolism.
2023-10-24 | PXD040894 | Pride
Project description:Prdm16 overexpression effect on inguinal white adipose tissue:stromal-vascular cells
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Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development. Brown adipose tissues were collected from Prdm16 knockout and wiletype mice with 4 biological replicates per condition. Experiment was done in two separate batch for 6-week-old and 11-month-old. Extracted RNA was hybridized to Agilent two-color arrays.
2014-04-09 | E-GEOD-55080 | biostudies-arrayexpress
Project description:Excess weight is associated with an increased risk of insulin resistance and type 2 diabetes. Activating thermogenic mechanisms is a potentially powerful means to reduce excess weight and achieve metabolic benefits. Recent studies show that cold stimuli trigger the conversion of white fat into beige fat, which can mediate non-shivering thermogenesis. The purpose of this study is to determine effect of chronic cold exposure on gene expression in iWAT. To this end, we performed RNA-sequencing of iWAT from mice at 30 ˚C or 7 ˚C for 3 weeks and identified significantly regulated genes under chronic cold in iWAT.
2021-12-14 | GSE133619 | GEO
Project description:Gene expression profile from brown adipose tissues of Prdm16 knockout and wile type mice. Prdm16 is a transcription factor that regulates the thermogenic gene program in brown and beige adipocytes. However, whether Prdm16 is required for the development or physiological function of brown adipose tissue (BAT) in vivo has been unclear. By analyzing mice that selectively lacked Prdm16 in the brown adipose lineage, we found that Prdm16 was dispensable for embryonic BAT development.
2014-04-09 | GSE55080 | GEO
Project description:Prdm16 is a transcription factor that drives a complete program of brown adipocyte differentiation, but the mechanism by which Prdm16 activates gene transcription remains unknown. Utilizing ChIP-seq teqhnique, we found that Prdm16 binds to chromatin at/near many brown fat-selective genes in BAT. Interestingly, Prdm16-deficiency dramatically reduced the binding of Med1 to Prdm16-target sites. Indeed, Prdm16 binds and recruits Med1 to BAT-enriched genes and the loss of Prdm16 caused a fundamental change in chromatin architecture at key BAT-selective genes and also reduced transcirptional activity. Moreover, Prdm16, through its interaction with Med1, defines and regulates the activity of super-enhancers that drive the expression of cell identity genes. Together, these data demonstrate that Prdm16 drives gene transcription by recruiting Med1 to control chromatin architecture and super-enhancers. Brown adipose tissues were collected from Prdm16 knockout and wiletype 9-month-old mice and ChIP-seq was performed for Prdm16, PolII, Med1, and H3K27ac.
2015-02-10 | E-GEOD-63965 | biostudies-arrayexpress
Project description:To investigate whether Cebpa-L1-AD-En2 produces a marked effect on adipogenesis in mouse adipose tissue, we injected the dCas9-KARB-En2 lentiviral system (iWAT_Cebpa-En2 group) or dCas9-KRAB-GFP (Control group) directly into mouse inguinal white adipose tissue (iWAT). We conducted RNA-seq analysis on the iWAT of iWAT-En2 group mice and control group mice at 13 weeks of age
2024-03-07 | GSE229849 | GEO
Project description:We asked if miRNAs are involved in PRDM16 protein expression. Thus microarray was employed with inguinal adipose tissues from contol, fasted and cold exposure C57BL/6J male mice In this dataset, we include all the miRNA expression data obtained from dissected mouse inguinal adipose tissues from control, fasted and cold exposure mice. Generally, microRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression at the post-transcriptional level. Based on previous results, we asked whether miRNAs are involved in the regulation of PRDM16 in ingWAT in response to different physiological stimuli. We therefore performed miRNA microarray analysis using ingWAT from the cold-exposed mice, the fasted mice and the control mice. Given that cold exposure increased the level of PRDM16 protein whereas fasting decreased its expression, miRNAs that have expression patterns opposite to that of PRDM16 were selectedã??
2015-11-07 | E-GEOD-74753 | biostudies-arrayexpress
Project description:Brown adipose tissue dissipates energy through heat and functions as a defense against cold and obesity. PPARγ ligands have been shown to induce the browning of white adipocytes; however, the underlying mechanisms remain unclear. Here we show that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose. These effects require expression of PRDM16, a factor that controls the development of classical brown fat. Depletion of PRDM16 blunts the effects of the PPARγ agonist rosiglitazone on the induced brown fat gene program. Conversely, PRDM16 and rosiglitazone synergistically activate the brown fat gene program in vivo. This synergy is tightly associated with an increased accumulation of PRDM16 protein, due in large measure to an increase in the half-life of the protein in agonist treated cells. Identifying compounds that stabilize PRDM16 protein may represent a novel therapeutic pathway for the treatment of obesity and diabetes. Microarray analysis of the differentiated inguinal adipocytes expressing sh-scr or sh-PRDM16 in the presence or absence of rosiglitazone (1uM). These samples were profiled using Affymetrix mouse 430A_2 arrays, representing 2 biological replicates for each samples (8 samples in total).
2012-03-06 | E-GEOD-35011 | biostudies-arrayexpress
Project description:Purpose: The goals of this experiment were to examine the transcriptional profiles (RNA-seq) of inguinal white adipose tissue (iWAT) in mice subjected to the indicated diets and treatments for eight weeks. Methods: 6-week-old C57BL6/J mice fed a control or a high-fat diet were treated with anti-PDGFcc neutralizing antibodies or Goat IgG for 2 weeks of treatment. Antibodies were administered by i.p. every two days. Four animals were treated in each condition. The resulting iWAT from these mice were sequenced in duplicates, aligned with STAR, quantified with featureCounts, and then differential gene expression analyses were performed using limma. Results: An unbiased analysis of hallmark pathways in iWAT of anti-PDGFcc antibody-treated mice and control animals using a pre-ranked Gene Set Enrichment Analysis (GSEA) identified adipogenesis as the pathway most differentially regulated by PDGFcc blockade when accounting for diet effects. By contrast, the hallmark fatty acid metabolism pathway which includes genes involved in lipid uptake, lipid oxidation, and lipid mobilization was not significantly enriched after anti-PDGFcc treatment. Similarly, hallmark pathways glycolysis, MTORC1 signaling, or TGFb signaling were not differentially regulated by anti-PDGFcc treatment after accounting for diet effects. An additional GSEA analysis of genes involved in lipid synthesis and storage identified a subset of genes up-regulated by PDGFcc blockade regardless of diet, which included several negative regulators of lipid synthesis and storage such as Insig1, Ppara, and Idh2. Conclusions: A GSEA identified adipogenesis as the pathway most differentially regulated by PDGFcc blockade when accounting for diet effects. Key genes involved included several negative regulators of lipid synthesis and storage such as Insig1, Ppara, and Idh2.
2021-03-20 | GSE169226 | GEO