Lysine-specific demethylase 1 target genes in brown adipocytes
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PROVIDER: PRJNA321978 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study is to identify the Lsd1 genome binding profile in brown adipocytes. Purpose: The aim of this study is to identify the Lsd1 genome binding profile in brown adipocytes. Methods: Libraries were prepared from Lsd1-immunoprecipitated DNA according to standard methods. ChIP-seq libraries were sequenced using a HiSeq 2000 (Illumina) and mapped to the mm10 reference genome using bowtie 2 (Langmead et al., 2009). Data were further analysed using the peak finding algorithm MACS 1.41 (Zhang et al., 2008) using input as control. All peaks with FDR greater than 0.3 % were excluded from further analysis. The uniquely mapped reads were used to generate the genome-wide intensity profiles, which were visualized using the IGV genome browser (Thorvaldsdottir et al., 2012). Results: HOMER (Heinz et al., 2010) was used to annotate peaks, to calculate overlaps between different peak files, and for motif searches. The genomic features (promoter, exon, intron, 3’ UTR, and intergenic regions) were defined and calculated using Refseq and HOMER. Genes annotated by HOMER were further used for a pathway analysis in WebGestalt (Heinz et al., 2010; Wang et al., 2013). ChIP-seq analysis revealed that Lsd1 was located at the promoter of 11735 genes.
2016-10-27 | GSE81556 | GEO
Project description:The adipose organ, including white and brown adipose tissues, is an important player in systemic energy homeostasis, storing excess energy in form of lipids while releasing energy upon various energy demands. Recent studies have demonstrated that white and brown adipocytes also function as endocrine cells and regulate systemic metabolism by secreting factors that act locally and systemically. However, a comparative proteomic analysis of secreted factors from white and brown adipocytes and their responsiveness to adrenergic stimulation has not been reported yet. Therefore, we studied and compared the secretome of white and brown adipocytes, with and without norepinephrine (NE) stimulation. Our results reveal that in the absence of NE, carbohydrate metabolism-regulating proteins are preferably secreted from white adipocytes, while brown adipocytes predominantly secrete integrin signaling proteins. Upon NE stimulation, white adipocytes secrete more proteins involved in lipid metabolism, while brown adipocytes secrete more proteins with specific anti-inflammatory properties. In conclusion, our study provides a comprehensive catalogue of novel adipokine candidates secreted from white and brown adipocytes with many of them responsive to NE.
2018-09-04 | PXD009280 | Pride
Project description:We have identified a population of adipocytes in fat tissue that arise from bone marrow-derived progenitor cells. We used microarrays to compare the global gene expression patterns of the bone marrow progenitor-derived adipocytes as well as conventional white and brown adipocytes to evaluate the relationship between these adipocyte subpopulations. Gonadal fat tissue (for white adipocytes) and intrascapular fat tissue (for brown adipocytes) was digested with collagenase and adipocytes were recovered by centrifugation/flotation. Bone marrow derived adipocytes were isolated from the adipocyte fraction of gonadal fat tissue from mice receiving bone marrow tranplants from donors expressing either green fluorescent protein (GFP) or beta-galactosidase (LacZ) by flow cytometry.
2010-01-08 | E-GEOD-19757 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-10-27 | GSE81557 | GEO
Project description:By screening a collection of epigenetic compounds, we find that Lysine-Specific Demethylase 1 (LSD1) inhibitors repress brown adipocyte differentiation. RNAi-mediated Lsd1 knockdown shows similar effect, which can be rescued by expression of wild-type, but not catalytically inactive, LSD1. Furthermore, adenoviral Cre-mediated LSD1 deletion in mice leads to inhibition of brown adipogenesis, validating the pivotal role of LSD1 in brown fat development in vivo. LSD1 is a histone H3 demethylase, which selectively removes methyl groups from mono- and di-methylated lysine 4 (H3K4me1 and H3K4me2) under most circumstances, and only from lysine 9 (H3K9me1/2) when bound with androgen receptor (AR) or estrogen receptor (ER). K4 demethylation causes transcription repression, while K9 demethylation may lead to activation of gene transcription. To investigate the target genes of LSD1 during BAT differentiaiton, we performed RNA-seq to profile the gene expression in brown adipocytes treated with DMSO or LSD1 inhibitor 611 (Cpd A) for 6 days, and gene set enrichment analysis (GSEA) was then employed to identify Gene Ontology (GO) terms that were significantly enriched.
2016-08-30 | GSE74900 | GEO
Project description:Blnc1 is a novel nuclear lncRNA that promotes brown and beige adipocyte differentiation and function. Blnc1 forms a ribonucleoprotein complex with transcription factor EBF2 to stimulate the thermogenic gene program. Further, Blnc1 itself is a target of EBF2, thereby forming a feedforward regulatory loop to drive adipogenesis toward thermogenic phenotype. We used microarrays to elucidate the role of Blnc1 on brown adipocyte differentiation and the induction of the thermogenic gene program. Brown adipocytes expressing vector or brown fat lncRNA 1 (blnc1) were differentiated for 6 days and harvested for RNA isolation and microarray using Affymetrix Mouse MG-430 PM Strip arrays. Two replicated samples were included in this study.
2015-02-28 | E-GEOD-55551 | biostudies-arrayexpress
Project description:We have identified a population of adipocytes in fat tissue that arise from bone marrow-derived progenitor cells. We used microarrays to compare the global gene expression patterns of the bone marrow progenitor-derived adipocytes as well as conventional white and brown adipocytes to evaluate the relationship between these adipocyte subpopulations.
2010-01-08 | GSE19757 | GEO
Project description:Cre recombinase activity was induced in differentiating brown adipocytes from CreERT2 Sykflox/flox mice in vitro, which resulted in a partial loss of Syk protein in mature brown adipocytes. Such cells were viable, morphologically normal and displayed largely normal gene expression as indicated by mRNA sequencing and qPCR analysis, suggesting that Syk is not required for survival and gene expression of terminally differentiated brown adipocytes. mRNA sequencing of Syk depleted brown adipocytes treated with 0.1 microM isoproterenol for 6 h showed that 2460 genes were not induced or suppressed upon stimulation. Gene set enrichment analysis revealed a great enrichment for genes essential for mitochondrial respiration and biogenesis, for genes associated with and required for adipogenesis, as well as for genes responsive to various stimuli in adipocytes among genes highly ranked by reduced fold changes in response to isoproterenol in the Syk deficient brown adipocytes.
2017-12-09 | GSE91081 | GEO
Project description:Brown adipose tissue (BAT) dissipates energy and promotes cardio-metabolic health4. However, loss of BAT during obesity and aging is a principal hurdle for BAT-centered obesity therapies. So far not much is known about BAT apoptosis and signals released by apoptotic brown adipocytes. Here, untargeted metabolomics demonstrated that apoptotic brown adipocytes release a specific pattern of metabolites with purine metabolites being highly enriched. Interestingly, this apoptotic secretome enhances expression of the thermogenic program in healthy adipocytes to maintain tissue functionality. This effect is mediated by the purine inosine which stimulates energy expenditure (EE) in brown adipocytes. Phosphoproteomic analysis demonstrated activation of the cAMP/protein kinase A signaling pathway and of pro-thermogenic transcription factors by inosine.
2022-05-31 | PXD032153 | Pride
Project description:miRNA array of a timecourse of 3T3-L1 differentiating into white adipocytes and C3H10T1/2 into brown adipocytes
2016-12-31 | GSE75697 | GEO