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Brown Adipogenic Reprogramming Induced by a Small Molecule

ABSTRACT: Transcriptome analysis of early adipogenesis induced by basal adipogenesis medium(AM) and AM+Bex for 2 days in C2C12 cells Global gene expression profiling has shown Bex induced adipogenic genes expression change

ORGANISM(S): Mus musculus

PROVIDER: GSE52364 | GEO | 2013/11/15

SECONDARY ACCESSION(S): PRJNA227500

REPOSITORIES: GEO

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Brown Adipogenic Reprogramming Induced by a Small Molecule

Project description:Transcriptome analysis of early adipogenesis induced by basal adipogenesis medium(AM) and AM+Bex for 2 days in C2C12 cells Global gene expression profiling has shown Bex induced adipogenic genes expression change We analyzed 4 samples from basal adipogenesis medium(AM) and AM+Bex(10uM) treated C2C12 cells using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed by Affymetrix Expression Console and Transcriptome Analysis Console (TAC) software.

2013-11-15 | E-GEOD-52364 | biostudies-arrayexpress

Human BMSCs protein analysis that interact with TRAF4 during adipogenic differentiation

Project description:To explore the mechanism underlying the negative regulation of adipogenesis by TRAF4, we performed the LC-MS/MS experiments to identify the proteins that interact with TRAF4 during adipogenic differentiation.

2020-05-27 | PXD017524 | Pride

Genome-wide maps of adipogenic TFs during brown preadipocyte differentiation

Project description:Enhancers play a central role in cell-type-specific gene expression and are marked by H3K4me1/2. Active enhancers are further marked by H3K27ac. However, the methyltransferases responsible for the deposition of H3K4me1/2 on enhancers remain elusive. Furthermore, the functions of these methyltransferases on enhancers and associated cell-type-specific gene expression are poorly understood. Here, we identify MLL4 (KMT2D) as a major H3K4 mono- and di-methyltransferase in mammalian cells. Using adipogenesis and myogenesis as model systems, we show that MLL4 exhibits cell-type- and differentiation-stage-specific genomic binding and is predominantly localized on enhancers. MLL4 co-localizes with lineage-determining transcription factors (TFs) on active enhancers during differentiation. Deletion of MLL4 dramatically decreases H3K4me1/2 and H3K27ac on enhancers and leads to severe defects in cell-type-specific gene expression and cell differentiation. Finally, we provide evidence that lineage-determining TFs recruit and require MLL4 to establish enhancers critical for cell-type-specific gene expression. Together, these results identify MLL4 as an H3K4 mono-/di-methyltransferase required for enhancer activation during cell differentiation. ChIP-Seq analyses of adipogenic TF (C/EBPalpha, C/EBPbeta, and PPARgamma) and Pol II profiles at D0 (day 0) and D2 (day 2) of adipogenesis in WT (MLL3-/-) and MLL4 KO (MLL3-/-;MLL4-/-) brown preadipocytes.

2013-12-17 | E-GEOD-50416 | biostudies-arrayexpress

Expression profiling of mouse bone marrow skeletal progenitors with osteogenic and adipogenic potential and adipogenic progenitors treated with IFNγ.

Project description:Bone marrow stromal cells (BMSCs) were isolated from the femora and tibiae of irtTA-GBD*-TAg transgenic mice. Using cellular cloning we established skeletal progenitors with unipotent osteogenic and adipogenic properties. Previous RNA-seq analysis of more progenitor types revealed differential expression in members of the Interferon-gamma (IFNγ) signaling pathway. Treatment of adipogenic progenitors with IFNγ inhibited adipogenesis and promoted osteogenesis. RNA-seq analysis of osteogenic, adipogenic and IFNγ treated adipogenic clones revealed factors controlling the osteogenic versus adipogenic commitment of bone marrow skeletal progenitors.

2018-07-02 | GSE114475 | GEO

Development of a 3D fatty infiltration platform to model, at higher scale, the impact of LY2090314 compound on fibro/adipogenic progenitor adipogenic drift

Project description:In human dystrophies, the progressive muscle wasting is exacerbated by ectopic deposition of fat and fibrous tissue originating from fibro/adipogenic progenitors (FAPs). In degenerating muscles, the ability of these cells to adjuvate a successful healing is attenuated and FAPs aberrantly expand and differentiate into adipocytes and fibroblasts. Thus, arresting the fibroadipogenic fate of FAPs, without affecting their physiological role, represents a valuable therapeutic strategy for patients affected by muscle diseases. Here, using a panel of adipose progenitor cells including human-derived FAPs coupled with pharmacological perturbations and proteome profiling, we report that LY2090314 interferes with a genuine adipogenic program acting as WNT surrogate for the stabilization of a competent -catenin transcriptional complex. To predict the beneficial impact of LY2090314 in limiting ectopic deposition of fat in human muscles, we combined the Poly-Ethylene-Glycol-Fibrinogen biomimetic matrix with these progenitor cells to create a miniaturized 3D model of adipogenesis. Using this scalable system, we demonstrated that a two-digit nanomolar dose of this compound is effective to repress adipogenesis in a higher 3D scale, thus offering a concrete proof for the use of LY2090314 to limit FAP-derived fat infiltrates in dystrophic muscles.

2023-06-13 | PXD040479 | Pride

Determination of Lsd1 function in C2C12 myoblast cells by global transcriptome analysis

Project description:First, we aimed to identify genes whose transcript levels change at the onset of myogenic versus adipogenic differentiation of muscle precursors. We therefore compared RNA-seq results obtained from C2C12 cells differentiated for 1 day in myogenic and adipogenic medium. Out of these genes, we wanted to determine those whose expression was affected by altered Lsd1 levels. To this end, we performed RNA-seq in C2C12 cells upon LSD1 overexpression and Lsd1 knock-down in adipogenic medium and compared them to corresponding control cells.

2017-12-15 | GSE98133 | GEO

AFF4 regulates cellular adipogenic differentiation via targeting autophagy

Project description:AFF4 was discovered as a scaffold protein of Super Elongation Complex (SEC) and exhibites an essential function on osteogenesis, tumorigenesis and odontogenesis. However, the adipogenic biological functions of AFF4 need further explorations. Here, we demonstrate that knockdown of AFF4 inhibits adipogenesis in both human mesenchymal stem cells (hMSCs) and lineage-committed 3T3-L1 preadipocytes. Conditional knocking down of Aff4 in transgenic mouse presents a thin body phenotype and impeded adipogenesis. Mechanistically, we define autophagy signaling as a crucial downstream of AFF4 through the combination of RNA-seq and ChIP-seq analyses. Depletion of AFF4 mediates the transcription of crutial autophagy genes ATG5 and ATG16L1. Simultaneous overexpression of ATG5 and ATG16L1 rescues the lineage commitment of AFF4-deficient cells. Our data elucidate that AFF4 is indispensable for adipogenic differentiation and reveal a novel mechanism for adipogenesis at transcriptional level.

2023-02-28 | GSE197354 | GEO

Expression data of genes and noncoding genes from the ADSCs and adipogenic-induced ADSCs

Project description:Adipogenesis participates in many physiological and pathological processes such as obesity and diabetes, and is regulated by a series of precise molecular events. However, the molecules involved in this regulation have not been fully characterized. We used microarrays to detail the full transcriptome expression profiles of undifferentiated and adipogenic-induced ADSCs.

2018-09-12 | GSE119796 | GEO

Comparing the miRNA transcriptome of FAPs cultured in basal medium (BM) and adipogenic differentiation medium (ADM)

Project description:Comparing the miRNA transcriptome of FAPs cultured in basal medium (BM) and adipogenic differentiation medium (ADM)

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Chidamide suppresses adipogenic differentiation of bone marrow derived mesenchymal stem cells

Project description:To explore the potential mechanism of chidamide in BM-MSC-mediated adipogenesis, we have employed mRNA microarray expression profiling platform to identify significant differential genes associated with adipogenic differentiation and chidamide management.

2022-04-13 | GSE199466 | GEO

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