Similar Datasets
Project description:The aims of the current study were to characterize the profile of circRNA during WATadipocytes adipogenesis.
2021-06-21 | GSE178502 | GEO
Project description:The aims of the current study were to characterize the effects of EGCG on mRNA transcriptome during WAT and BAT adipocytes adipogenesis.
2021-05-03 | GSE173710 | GEO
Project description:Circular RNA Expression Profiles during brown adipogenesis
| PRJNA755181 | ENA
Project description:Histone H3K4me1/2 methyltransferases MLL3/MLL4 and H3K27 acetyltransferases CBP/p300 are major enhancer epigenomic writers. To understand how these epigenomic writers orchestrate enhancer landscapes during cell differentiation, we have profiled genomic binding of MLL4, CBP, lineage-determining transcription factors, as well as transcriptome and epigenome during adipogenesis of immortalized preadipocytes derived from mouse brown adipose tissue (BAT). We show that MLL4 and CBP drive the dynamic enhancer epigenome, which correlates with the dynamic transcriptome. MLL3/MLL4 are required for CBP/p300 binding on enhancers activated during adipogenesis. Further, we show that MLL4 and CBP identify super-enhancers of adipogenesis and that MLL3/MLL4 are required for the formation of super-enhancers. Finally, in brown adipocytes differentiated in culture, MLL4 identifies primed super-enhancers of genes fully activated in BAT such as the thermogenic Ucp1. Comparison of MLL4-defined super-enhancers in brown and white adipogenesis predicted a list of brown-specific super-enhancers SEs associated genes that are likely to be important to BAT functions. These results establish MLL3/MLL4 and CBP/p300 as master enhancer epigenomic writers and suggest that enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation. Our data also provide a rich resource for understanding epigenomic regulation of brown adipogenesis.
2017-01-01 | GSE74189 | GEO
Project description:We performed a genome-wide deep sequencing analysis of the microRNAs abundant in mesenchymal stem cells (MSCs) derived from murine brown adipose tissue and in in vitro differentiated mature brown adipocytes. Several microRNAs were identified as differentially regulated when comparing datasets from MSCs vs. mature fat cells. These microRNAs may have an implication in the regulation of adipogenesis as well as thermogenesis in brown adipose tissue (BAT). Examination of BAT-derived MSCs (BAT-MSC; 1 sample) and in vitro differentiated mature brown fat cells (BAT-DIFF; 1 sample) vertis biotechnologie AG, D-85354 Freising, Germany (library construction and sequencing)
2013-05-28 | E-GEOD-45499 | biostudies-arrayexpress
Project description:Recents studies in mice and humans demonstrated the relevance of H2S-synthesising enzymes (such as CTH, CBS and MPST) in adipose tissue physiology and preadipocyte differentiation into adipocytes. Here, we aimed to investigate the combined role of CTH, CBS and MPST in the preservation of adipocyte protein persulfidation and adipogenesis. Joint CTH, CBS and MPST gene knockdown was achieved treating fully human adipocytes with siRNAs against these transcripts (siRNA_MIX). Adipocyte protein persulfidation was analyzed by a mass spectrometry label-free quantitative approach coupled with a dimedone-switch method for protein labeling and purification. The proteomic analysis quantified 216 proteins with statistically different persulfidation levels in KD cells compared to control adipocytes. In fully differentiated adipocytes, CBS and MPST mRNA and protein levels were abundant, whereas CTH expression was very low. Of note, siRNA_MIX administration resulted in a significant decrease in CBS and MPST expression, without impacting on CTH. Dual CBS and MPST gene knockdown resulted in decreased expression of relevant genes for adipocyte biology, including adipogenesis, mitochondrial biogenesis and lipogenesis, but increased proinflammatory- and senescence-related genes, in parallel to a significant disruption in adipocyte protein persulfidation pattern. While among less persulfidated proteins, we identified several relevant proteins for adipocyte adipogenesis and function, among the most persulfidated, key mediators of adipocyte inflammation and dysfunction, but also some proteins that might have a positive role of adipogenesis were found. In conclusion, current study indicates that joint knockdown of CBS and MPST (but not CTH) in adipocytes impairs adipogenesis and promotes inflammation, possibly by disrupting the pattern of protein persulfidation in these cells, and suggesting that these enzymes were required for the functional maintenance of adipocytes.
2022-08-12 | PXD032370 | Pride
Project description:We performed a genome-wide deep sequencing analysis of the microRNAs abundant in mesenchymal stem cells (MSCs) derived from murine brown adipose tissue and in in vitro differentiated mature brown adipocytes. Several microRNAs were identified as differentially regulated when comparing datasets from MSCs vs. mature fat cells. These microRNAs may have an implication in the regulation of adipogenesis as well as thermogenesis in brown adipose tissue (BAT).
2013-05-28 | GSE45499 | GEO
Project description:Increasing energy expenditure by promoting the thermogenic program in brown adipocytes is a promising approach to combat human obesity. To fully exploit the potential of this approach a comprehensive understanding of the gene regulatory network that controls both lineage commitment and differentiation of brown cells is necessary. Here, we systematically examine the transcriptomic and epigenomic transitions from mesenchymal stem cells to brown adipocytes (BA) and we perform a comparative analysis with differentiating white adipocytes (WA). We identify coding genes, lncRNA genes, and microRNA genes that are differentially regulated upon BA differentiation. In addition, we generate genome wide reference maps for several chromatin marks throughout brown adipogenesis. We identify putative (super-)enhancers, super-enhancers controlled genes in brown and white adipocytes, as well as target genes of the brown lineage-committing factor BMP7. Finally we show that overexpression and knockdown of four putative novel adipogenic regulators (the kinase Pim1, and the transcription factors Six1, Rreb1, and Sox13), indeed affects BA differentiation, suggesting an important role in brown adipogenesis.
2016-12-31 | GSE75639 | GEO
Project description:Increases in organismal energy expenditure, as during cold exposure or exercise training, can improve metabolic health. This process is dependent also on brown adipose tissue (BAT) thermogenesis in mice and humans. Understanding and harnessing the molecular circuits activating BAT function is thus of great interest to devise novel approaches to counteract obesity and type 2 diabetes (T2D). In contrast to protein-coding genes, the role of long noncoding RNAs (lncRNAs) during BAT differentiation and function remains poorly understood. To address this, we performed RNA-Seq and identified the maternal allele-specific (imprinted) lncRNA H19 increased upon cold-mediated BAT activation and decreased upon chronic diet-induced obesity (DIO) BAT dysfunction. An inverse correlation of H19 expression with body-mass indices (BMI) was observed in a cohort of >160 lean and obese humans. H19 silencing impaired adipogenesis and oxidative metabolism in brown but not white adipocytes, while H19 gain-of-function increased nutrient oxidation and mitochondrial respiration, thus supporting a BAT-regulatory role for H19. In vivo H19 overexpression protected against DIO, improved insulin sensitivity and rescued DIO-mediated defects in energy expenditure in conjunction with improved mitochondrial biogenesis. In contrast, BAT-selective H19 loss decreased energy dissipation and sensitized towards high fat diet-induced body weight gains. When investigating other parent-of-origin specific, monoallelically expressed genes, we strikingly observed that paternally expressed genes (PEGs) were largely absent from BAT and coordinately downregulated during brown adipogenesis, whilst the same gene set was robustly expressed in white fat stores, a phenomenon not observed for maternally expressed genes (MEGs). Using H19 loss- and gain-of-function in primary adipocytes, we demonstrate that H19 acts as ‘PEG gatekeeper’ in brown, not white adipocytes, potentially due to recruitment of PEG-inactivating H19-MBD1 complexes in mature brown adipocytes. The exclusive PEG expression in white adipose tissuer could underly the observed susceptibility of mice exhibiting high PEG abundances towards DIO-evoked weight gain. Collectively, we here define novel roles for the imprinted lncRNA H19 in brown adipocyte differentiation and function in vitro, control of energy expenditure in vivo and repression of paternal allele-specific gene expression in BAT. This has far-reaching implications for our understanding of how monoallelical gene expression affects metabolic eustasis in both rodent models and, potentially, human patients.
2018-06-26 | GSE116225 | GEO
Project description:Increases in organismal energy expenditure, as during cold exposure or exercise training, can improve metabolic health. This process is dependent also on brown adipose tissue (BAT) thermogenesis in mice and humans. Understanding and harnessing the molecular circuits activating BAT function is thus of great interest to devise novel approaches to counteract obesity and type 2 diabetes (T2D). In contrast to protein-coding genes, the role of long noncoding RNAs (lncRNAs) during BAT differentiation and function remains poorly understood. To address this, we performed RNA-Seq and identified the maternal allele-specific (imprinted) lncRNA H19 increased upon cold-mediated BAT activation and decreased upon chronic diet-induced obesity (DIO) BAT dysfunction. An inverse correlation of H19 expression with body-mass indices (BMI) was observed in a cohort of >160 lean and obese humans. H19 silencing impaired adipogenesis and oxidative metabolism in brown but not white adipocytes, while H19 gain-of-function increased nutrient oxidation and mitochondrial respiration, thus supporting a BAT-regulatory role for H19. In vivo H19 overexpression protected against DIO, improved insulin sensitivity and rescued DIO-mediated defects in energy expenditure in conjunction with improved mitochondrial biogenesis. In contrast, BAT-selective H19 loss decreased energy dissipation and sensitized towards high fat diet-induced body weight gains. When investigating other parent-of-origin specific, monoallelically expressed genes, we strikingly observed that paternally expressed genes (PEGs) were largely absent from BAT and coordinately downregulated during brown adipogenesis, whilst the same gene set was robustly expressed in white fat stores, a phenomenon not observed for maternally expressed genes (MEGs). Using H19 loss- and gain-of-function in primary adipocytes, we demonstrate that H19 acts as ‘PEG gatekeeper’ in brown, not white adipocytes, potentially due to recruitment of PEG-inactivating H19-MBD1 complexes in mature brown adipocytes. The exclusive PEG expression in white adipose tissuer could underly the observed susceptibility of mice exhibiting high PEG abundances towards DIO-evoked weight gain. Collectively, we here define novel roles for the imprinted lncRNA H19 in brown adipocyte differentiation and function in vitro, control of energy expenditure in vivo and repression of paternal allele-specific gene expression in BAT. This has far-reaching implications for our understanding of how monoallelical gene expression affects metabolic eustasis in both rodent models and, potentially, human patients.
2018-06-26 | GSE116226 | GEO