High throughput analysis of three human adipose cell lines PAZ6, SGBS and SW872
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE63190 | GEO | 2015/01/01
SECONDARY ACCESSION(S): PRJNA266964
REPOSITORIES: GEO
Similar Datasets
Project description:We report molecular characterization of human brown and white adipocytes. We showed that PAZ6 and SW872 cells exhibit classical molecular and phenotypic markers of brown and white adipocytes, respectively. However, SGBS cells presented a versatile phenotype of adipocyte Sequencing of three human adipocytes cell lines (SGBS, SW872 and PAZ6) in undifferentiated and differentiated stages.
2015-01-01 | E-GEOD-63190 | 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. 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:Hypoxia in adipose tissue is suggested to be involved in the development of a chronic mild inflammation, which in obesity can further lead to insulin-resistance. The effect of hypoxia on gene expression in adipocytes seems to play a central role in this inflammatory response observed in obesity. However, the global impact of hypoxia on transcriptional changes in human adipocytes is unclear. Therefore, we compared gene expression profiles of human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes under normoxic or hypoxic conditions to detect hypoxia-responsive genes in adipocytes by using whole human genome microarrays. Human SGBS adipocytes were cultured in a hypoxic environment (1% O2) for 3, 6 and 16 hours and the control group was cultured under normoxic conditions (21% O2). Total RNA was prepared from control and treated SGBS cells, in triplicate experiments, and probes were hybridized on ‘Human Genome U133 2.0’ arrays (Affymetrix).
2011-04-14 | E-GEOD-28603 | biostudies-arrayexpress
Project description:Brown adipose tissue is specialized to burn lipids for heat generation as a natural defense against cold and obesity. Previous studies established microRNAs as essential regulators of brown adipocyte differentiation, but it remains unknown whether microRNAs are required for the feature maintenance of mature brown adipocytes. To address this question, we ablated Dgcr8, a key regulator of the microRNA biogenesis pathway, in mature brown as well as white adipocytes. The adipose tissue -specific Dgcr8 knockout mice displayed enlarged but pale interscapular brown fat with decreased expression of genes characteristic of brown fat, and the mice were intolerant to cold exposure. In vitro primary brown adipocyte cultures confirmed that microRNAs are required for marker gene expression in mature brown adipocytes. We also demonstrated that microRNAs are essential for the browning of subcutaneous white adipocyte both in vitro and in vivo. Using this animal model, we performed microRNA expression profiling analysis and identified a set of BAT-specific microRNAs that are up-regulated during brown adipocyte differentiation and enriched in brown fat compared to other organs. We identified miR-182 and miR-203 as new regulators of brown adipocyte development. Taken together, our study demonstrates an essential role of microRNAs in the maintenance as well as the differentiation of brown adipocytes.
2014-08-07 | GSE60165 | GEO
Project description:Attainment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and increased energy expenditure potential, is a legitimate strategy for combating obesity. The unique transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our ability to promote brown adipogenesis over white. In the present work, we used microarray analysis strategies to study primary preadipocytes, and we made the striking discovery that brown preadipocytes demonstrate a myogenic transcriptional signature, whereas both brown and white primary preadipocytes demonstrate signatures distinct from those found in immortalized adipogenic models. We found a plausible SIRT1-related transcriptional signature during brown adipocyte differentiation that may contribute to silencing the myogenic signature. In contrast to brown preadipocytes or skeletal muscle cells, white preadipocytes express Tcf21, a transcription factor that has been shown to suppress myogenesis and nuclear receptor activity. In addition, we identified a number of developmental genes that are differentially expressed between brown and white preadipocytes and that have recently been implicated in human obesity. The interlinkage between the myocyte and the brown preadipocyte confirms the distinct origin for brown versus white adipose tissue and also represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid catabolism rather than storage, much like oxidative skeletal muscle tissue. Experiment Overall Design: Comparisons of white and brown pre- and mature-adiposytes
2009-04-08 | E-GEOD-7032 | biostudies-arrayexpress
Project description:Most information on molecular processes accompanying and driving adipocyte differentiation are derived from rodent models. Here, a comprehensive analysis of combined transcriptomic and proteomic alterations during adipocyte differentiation in Simpson–Golabi–Behmel Syndrome (SGBS) cells is provided. The SGBS cells are a well-established and the most widely applied cell model to study human adipocyte differentiation and cell biology. However, the molecular alterations during human adipocyte differentiation in SGBS cells have not yet been described in a combined analysis of proteome and transcriptome. Here a global proteomic and transcriptomic data set comprising relative quantification of a total of 14372 mRNA transcripts and 2641 intracellular and secreted proteins is presented. 1153 proteins and 313 genes are determined as differentially expressed between preadipocytes and the fully differentiated cells including adiponectin, lipoprotein lipase, fatty acid binding protein 4, fatty acid synthase, stearoyl-CoA desaturase, and apolipoprotein E and many other proteins from the fatty acid synthesis, amino acid synthesis as well as glucose and lipid metabolic pathways. Preadipocyte markers, such as latexin, GATA6, and CXCL6, are found to be significantly downregulated at the protein and transcript level. This multi-omics data set provides a deep molecular profile of adipogenesis and will support future studies to understand adipocyte function.
2020-05-25 | GSE123385 | GEO
Project description:Brown adipose tissue is specialized to burn lipids for heat generation as a natural defense against cold and obesity. Previous studies established microRNAs as essential regulators of brown adipocyte differentiation, but it remains unknown whether microRNAs are required for the feature maintenance of mature brown adipocytes. To address this question, we ablated Dgcr8, a key regulator of the microRNA biogenesis pathway, in mature brown as well as white adipocytes. The adipose tissue -specific Dgcr8 knockout mice displayed enlarged but pale interscapular brown fat with decreased expression of genes characteristic of brown fat, and the mice were intolerant to cold exposure. In vitro primary brown adipocyte cultures confirmed that microRNAs are required for marker gene expression in mature brown adipocytes. We also demonstrated that microRNAs are essential for the browning of subcutaneous white adipocyte both in vitro and in vivo. Using this animal model, we performed microRNA expression profiling analysis and identified a set of BAT-specific microRNAs that are up-regulated during brown adipocyte differentiation and enriched in brown fat compared to other organs. We identified miR-182 and miR-203 as new regulators of brown adipocyte development. Taken together, our study demonstrates an essential role of microRNAs in the maintenance as well as the differentiation of brown adipocytes. TotalRNAs were extracted using a Qiagen kit, and 5 M-NM-<g of total RNAs for each sample were used to prepare the mRNA- Seq library according to the manufacturerM-bM-^@M-^Ys instruction (NEB). cDNA libraries were prepared and sequenced by Hi-seq in Whitehead Genome Core. 2 replicates of each treatment were analyzed.
2014-08-07 | E-GEOD-60165 | biostudies-arrayexpress
Project description:Adipose tissue is the major depot for energy storage. Recent studies have shown that at least three types of adipocytes can be distinguished depending on their anatomical locations : 1) The classic brown adipocytes, i.e., brown adipose tissue (BAT); 2) The 'brite' (brown-in-white) adipocytes, i.e. inguinal white adipose tissue (iWAT); 3) The 'true' white adipocytes, i.e., epididymal white adipose tissue (eWAT). Two strains of mice (SV129 and C57BL/6J) were used in this study. SV strain is resistant to obesity and latter is prone to obesity. Pre-adipocyte cells were isolated from subcutaneous tissue (iWAT) to create four groups of cell cultures per strain of mouse.
2016-04-20 | GSE57903 | GEO
Project description:Attainment of a brown adipocyte cell phenotype in white adipocytes, with their abundant mitochondria and increased energy expenditure potential, is a legitimate strategy for combating obesity. The unique transcriptional regulators of the primary brown adipocyte phenotype are unknown, limiting our ability to promote brown adipogenesis over white. In the present work, we used microarray analysis strategies to study primary preadipocytes, and we made the striking discovery that brown preadipocytes demonstrate a myogenic transcriptional signature, whereas both brown and white primary preadipocytes demonstrate signatures distinct from those found in immortalized adipogenic models. We found a plausible SIRT1-related transcriptional signature during brown adipocyte differentiation that may contribute to silencing the myogenic signature. In contrast to brown preadipocytes or skeletal muscle cells, white preadipocytes express Tcf21, a transcription factor that has been shown to suppress myogenesis and nuclear receptor activity. In addition, we identified a number of developmental genes that are differentially expressed between brown and white preadipocytes and that have recently been implicated in human obesity. The interlinkage between the myocyte and the brown preadipocyte confirms the distinct origin for brown versus white adipose tissue and also represents a plausible explanation as to why brown adipocytes ultimately specialize in lipid catabolism rather than storage, much like oxidative skeletal muscle tissue. Keywords: In vitro differentiation
2007-05-31 | GSE7032 | GEO
Project description:Brown adipose tissue (BAT) is a central thermogenic organ that enhances energy expenditure (EE) and cardiometabolic health. However, regulators that specifically increase the number of thermogenic adipocytes are still an unmet need. Here, we show by phosphoproteomics that cAMP activates distinct signaling pathways in brown progenitors, with the cAMP-EPAC1 axis enhancing proliferation and differentiation of thermogenic but not white adipocytes. Further analysis revealed that a specific subpopulation of preadipocytes that are PDGFRα-positive express EPAC1. In vivo, pharmacological activation of EPAC1 enhances BAT growth and browning of white fat, leading to increased EE and reduced diet-induced adiposity. In contrast, mice lacking EPAC1 in PDGFRα-positive preadipocytes show the opposite phenotype. Importantly, EPAC1 activation enhances proliferation and differentiation of human brown adipocytes and human brown fat organoids. Interestingly, a coding variant in EPAC1 that positively correlates with BMI abolishes norepinephrine-induced proliferation of brown adipocytes. Thus, EPAC1 might be an attractive target to enhance thermogenic adipocyte number and EE to combat metabolic diseases.
2023-11-11 | PXD046709 | Pride