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Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [expression profiling]

ABSTRACT: To investgate the role of EBF1 in human adipocyte, we performed global expression profiling in human adipocytes transfected with siRNA targeting EBF1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42680 | GEO | 2014/05/22

SECONDARY ACCESSION(S): PRJNA182725

REPOSITORIES: GEO

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Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [expression profiling]

Project description:To investgate the role of EBF1 in human adipocyte, we performed global expression profiling in human adipocytes transfected with siRNA targeting EBF1. Human adipocytes differentiated in vitro were transfected with siRNA targeting EBF1 or Non-targeting Control. The cells were incubated for approximately 48 hours upon which Total RNA were purified. Gene expression profiling was performed using Affymetrix Human Gene 1.1 ST arrays (Affymetrix, Inc., Santa Clara, CA). Data were analyzed with packages available from Bioconductor (www.bioconductor.org). Normalization and calculation of gene expression was performed with the Robust Multichip Average expression measure using oligo package. Prior to further analysis, a non-specific filter was applied to include genes with expression signal >30 in at least 20% of all samples. A total of three independent transfection experiments were performed for the pre-adipocytes obtained from one donor. Same experiment were repeated with cells from another donor.

2014-05-22 | E-GEOD-42680 | biostudies-arrayexpress

Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [ChIP-seq]

Project description:Examination of EBf1 binding by ChIP-seq in differentiated human adipose stromal cell (hASC) pre-adipocyte Pre-Adipocytes differentiated in-vitro were fixed in 1% formaldehyde for 15 min at room temperature and quenched for 5 min by adding glycine to a final concentration of 0.125 M. ChIP assays were then performed with custom-made EBF1 antibody or rabbit IgG . ChIP-sequencing libraries were prepared using NEBnext chip-seq library Prep master mix set from 5 ng of anti-EBF1 and anti-IgG ChIP DNA, respectively. Sequence data were generated with Illumina HiSeq 2000 single-read sequencing and aligned against the human genome (hg19, NCBI).

2014-05-22 | E-GEOD-54889 | biostudies-arrayexpress

Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [ChIP-seq]

Project description:Examination of EBf1 binding by ChIP-seq in differentiated human adipose stromal cell (hASC) pre-adipocyte

2014-05-22 | GSE54889 | GEO

Early B cell factor 1 regulates adipocyte morphology and lipolysis in white adipose tissue.

Project description: Not available

| S-EPMC4109056 | biostudies-literature

Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-22 | E-GEOD-54890 | biostudies-arrayexpress

Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-05-22 | GSE54890 | GEO

Tumoral acidosis promotes adipose tissue depletion by fostering adipocyte lipolysis

Project description:Adaptation to acidosis has been reported to induce a shift towards fatty acid metabolism. We observed that conditioned medium of HCT, FaDu and SiHa adapted to acidosis (pH6.5) induced higher lipolysis of primary subcutaneous and mesenteric adipocytes compared to cancer cells maintained at pH7.4. In order to identify the prolipolytic factors induced by acidosis, we examined the differences between cancer cells adapted to pH6.5 and those maintained at pH7.4 by RNA sequencing. Cancer cells adapted to pH6.5 showed profound alterations in their gene expression compared with cancer cells maintained at pH7.4. Here, we focused on predicted secreted genes. We determined that 84 altered genes predicted to be secreted proteins overlapped between the 3 cancer cell lines, 24 of which were overexpressed. The role of these overexpressed genes was determined in vitro. We studied their role in inducing adipocyte lipolysis and in the depletion of adipose tissue observed in cancer cachexia.

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Brown and white adipocyte differentiation

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

mRNA profiling of MEST knockdown in human adipocyte precursor cells at early stage (day 3) of adipocyte differentiation

Project description:The Mesoderm-specific transcript homolog protein MEST is a member of the alpha/beta hydrolase fold family that is expressed in adipose tissue, adipocytes as well as their precursor cells. To get an idea about potential functions of MEST in adipocyte development, we knocked down MEST in human Multipotent Adipose-Derived Stem (hMADS) cells, induced adipocyte differentiation by a chemically defined medium and performed gene expression profiling at the early stage of adipocyte differentiation. Two-condition experiment, hMADS cells at day 3 after induction of adipocyte differentiation, comparison of cells transfected with an siRNA targeting MEST (siMEST) to cells transfected with a control siRNA (siC). Biological replicates: 3, indepently grown and harvested. On each array, one biological replicate of siMEST-transfected cells was directly compared to one biological replicate os siC-transfected cells (serving as reference sample). All hybridizations were repeated with reversed dye assignment (dye-swap) as technical replicates.

2015-06-24 | E-GEOD-63132 | biostudies-arrayexpress

Adipocyte p53 coordinates the adipose tissue immune cell landscape upon intermittent fasting

Project description:In obesity, sustained adipose tissue (AT) inflammation constitutes a cellular memory that limits the effectiveness of weight loss interventions. Yet, its fasting regimen-dependent regulation is unknown. Here, we show that cyclic intermittent fasting (IF) exacerbates the lipid-associated macrophage (LAM) inflammatory phenotype of visceral AT in obese mice. Importantly, we provide evidence that this increase in LAM abundance is almost entirely dependent on p53-driven adipocyte apoptosis. Adipocyte-specific deletion of p53 prevents LAM accumulation in AT during IF and increases the catabolic state of adipocytes, ameliorates metabolic flexibility, and insulin sensitivity. Finally, in cohorts of obese/diabetic patients, we describe a p53 polymorphism that links to long-term efficacy of a fasting-mimicking diet and that the expression of LAM markers and p53 in AT negatively correlates with maintaining weight loss after bariatric surgery. Overall, our results demonstrate that p53 signaling in adipocytes dictates LAM accumulation in AT under IF and that adipocyte p53 modulates fasting effectiveness in mice and humans.

2024-01-16 | PXD041351 | Pride

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