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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene

ABSTRACT: Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. BHC80 protein, encoded by phf21a gene, is a part of LSD1 histone demethylase complex and is essential for the demethylation activity. To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in BHC80-deficient 3T3-L1 cells 3T3-L1 preadipocytes were transfected with either BHC80-specific siRNA or control siRNA (siGL3). 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction.

ORGANISM(S): Mus musculus

SUBMITTER: Mitsuyoshi Nakao

PROVIDER: E-GEOD-18599 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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FAD-dependent lysine-specific demethylase-1 regulates cellular energy expenditure.

Hino Shinjiro S Sakamoto Akihisa A Nagaoka Katsuya K Anan Kotaro K Wang Yuqing Y Mimasu Shinya S Umehara Takashi T Yokoyama Shigeyuki S Kosai Ken-Ichiro K Nakao Mitsuyoshi M

Nature communications 20120327

Environmental factors such as nutritional state may act on the epigenome that consequently contributes to the metabolic adaptation of cells and the organisms. The lysine-specific demethylase-1 (LSD1) is a unique nuclear protein that utilizes flavin adenosine dinucleotide (FAD) as a cofactor. Here we show that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. We find that the loss of LSD1 function, either by short interfering RNA or b ...[more]

PMID: 22453831

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Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine

Project description:Adipogenic differentiation and metabolic adaptation are initiated through transcriptional and epigenetic reprogramming. In particular, dynamic changes in histone modifications may play central roles in the rearrangement of gene expression patterns. LSD1 (KDM1) protein, encoded by aof2 gene, is a histone demethylase, which is involved in transcriptional regulation. Since the enzymatic activity of LSD1 is FAD (flavin adenine dinucleotide)-dependent, its effects on gene expression may be influenced by FAD availability. To address the importance of histone demethylation in adipogenic differentiation and function, we performed cDNA microarray in LSD1-deficient 3T3-L1 cells as well as in the cells treated with LSD1 inhibitor tranylcypromine (TC). FAD-synthesizing enyme, riboflavin kinase (RFK) -deficient cells were also subjected to the microarray analysis. 3T3-L1 preadipocytes were transfected with aof2- or rfk- specific siRNA or control siRNA (siGL3) . 24 hours later, cells were subjected to adipogenic induction. 24 hours later, cells were harvested for total RNA extraction. For the TC treatment, TC was added to the adipogenic induction medium.

2012-04-04 | E-GEOD-18598 | biostudies-arrayexpress

Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene

2012-04-05 | GSE18599 | GEO

Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine

2012-04-05 | GSE18598 | GEO

Importance of histone demethylation in adipogenic differentiation and function

Project description:This SuperSeries is composed of the following subset Series: GSE18598: Differentiating 3T3-L1 adipocytes, introduced with siRNA against aof2 and rfk genes, or treated with tranylcypromine GSE18599: Differentiating 3T3-L1 adipocytes, introduced with siRNA against phf21a gene Refer to individual Series

2012-04-04 | E-GEOD-18600 | biostudies-arrayexpress

Expression data from 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells

Project description:Bivalent H3K4me3 and H3K27me3 chromatin domains in embryonic stem cells keep active developmental regulatory genes expressed at very low levels and poised for activation. Here, we show an alternative and previously unknown bivalent modified histone signature in lineage-committed mesenchymal stem cells and preadipocytes that pairs H3K4me3 with H3K9me3 to maintain adipogenic master regulatory genes (Cebpa and Pparg) expressed at low levels yet poised for activation when differentiation is required. We show lineage-specific gene-body DNA methylation recruits H3K9 methyltransferase SETDB1 which methylates H3K9 immediately downstream of transcription start sites marked with H3K4me3 to establish the bivalent domain. At the Cebpa locus, this prevents transcription factor C/EBPÎ² binding, histone acetylation, and further H3K4me3 deposition and is associated with pausing of RNA polymerase II, which limits Cebpa gene expression and adipogenesis. We used microarrays to detail the global programme of gene expression in 3T3-L1 preadipocytes and 10Th1lf mesenchymal stem cells and identified up-regulated genes upon knockdown of SETDB1, MBD1, and MCAF1. SETDB1, MBD1, or MCAF1 was knocked-down in 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells for RNA extraction and hybridization on Affymetrix microarrays. Small interfering RNAs (siRNA) targeting to Setdb1, Mbd1, or Mcaf1 was transfected to 3T3-L1 preadipocytes or 10Thalf mesenchymal stem cells.

2015-11-19 | E-GEOD-73231 | biostudies-arrayexpress

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation

Project description:We used the 3T3-L1 preadipocyte cell line (Green and Kehinde. Cell 5:19-25, 1974; ATCC CL-173), in which adipogenic differentiation is experimentally induced when quiescent 3T3-L1 cells are incubated with serum and IDX (insulin, dexamethasone, isobutylmethylxanthine). Following IDX addition, the cells retract and re-enter the cell cycle in the so-called clonal expansion phase. Two to three days later the cells definitively exit the cell cycle, express adipocyte-specific genes, and accumulate lipids to form lipid droplets. 3T3-L1 cells were grown in DMEM/FBS 10% until they reached confluence and entred quiescence following contact inhibition. The cells were kept confluent in the same medium for 2 days. The medium was renewed and supplemented with IDX for 48 hours. The medium was supplemented with insulin and renewed every 2 days until the adipogenic differentiation was completed.

2015-01-01 | E-GEOD-50612 | biostudies-arrayexpress

A systems-level approach to parental genomic imprinting: the imprinted gene network includes extracellular matrix genes and regulates cell cycle exit and differentiation

2015-01-01 | GSE50612 | GEO

Chromatin interaction of Cebpa during adipocyte differentiation (4C-Seq)

Project description:Cebpa is a critical transcription factor gene for adipocyte differentiation and adipose tissue development. However, mechanisms controlling Cebpa expression during adipogenic differentiation remain largely unknown. Here, we generated the high-resolution chromatin interaction maps of Cebpa in 3T3-L1 preadipocytes (3T3-L1) and 3T3-L1 adipocytes (3T3-L1-AD) using circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq), and characterized differences in their chromatin interactomes and chromatin status of the interaction sites during adipogenic differentiation. We performed a 4C-seq experiment on inguinal white adipose tissue (iWAT) to evaluate whether chromatin interaction between Cebpa-L1-AD-En2 and Cebpa promoters in 3T3-L1 adipocytes also exists in mouse adipose tissue.

2024-03-07 | GSE222688 | GEO

Epigenomic profiling of 3T3-L1 adipogenesis

Project description:3T3-L1 pre-adipocyte cells were grown to confluence and induced to differentiate in adipogenic media. Examination of 6 histone modifications and CTCF at 4 time points and PPARG at 1 time point using ChIP-Seq

2010-09-30 | E-GEOD-21365 | biostudies-arrayexpress

Development of gene expression signatures for contact-inhibited and adipogenic-differentiated 3T3-L1 and NIH3T3 fibroblasts

Project description:Given previous works showing that, in the process of adipogenic differentiation of 3T3-L1 fibroblasts, the cells need to be cultured to confluency followed by additional incubation before initiating differentiation, we hypothesized that contact inhibition of proliferation (CIP) is requisite for making the cells prone to the differentiation. We screened upregulated genes in contact-inhibited 3T3-L1 fibroblasts, as well as NIH3T3 fibroblasts that are also sensitive to contact inhibition, by a whole genome microarray analysis. We also screened the genes that undergo rapid downregulation after the initiation of adipogenic differentiation. To investigate the mechanism of contact inhibition of proliferation and adipogenic differentiation of 3T3-L1 and NIH3T3 fibroblasts, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish proliferating and contact-inhibited cells and cells that undergo adipogenic differentiation. Total RNAs from 80% confluent (3T3-L1_80%, NIH3T3_80%) and overconfluent (3T3-L1_overconfluent, NIH3T3_overconfluent) cells and cells stimulated with the adipogenic differentiation medium (ZenBio) for 2 hours (3T3-L1_adipo diff med 2 hours, NIH3T3_adipo diff med 2 hours) were harvested and subjected to the microarray analysis.

2015-05-28 | E-GEOD-69320 | biostudies-arrayexpress

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