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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE50612 | GEO | 2015/01/01

SECONDARY ACCESSION(S): PRJNA218101

REPOSITORIES: GEO

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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

Transcription profiling of mouse 3T3-L1 tissue (preadipocytes) treated with trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA)

Project description:Trans-10, Cis-12 conjugated linoleic acid (t10c12 CLA) causes fat loss in mouse white adipose tissue (WAT) and 3T3-L1 adipocyte tissue culture; however in preadipocyte tissue (this series) the UPS/ISR and fat loss is not detected. The early transcriptome changes in 3T3-L1 preadipocyte tissue culture were analyzed using high-density microarrays to better characterize the signaling pathways responding to t10c12 CLA. Their gene expression responses between 4 to 12 hr after treatment do not show a set of genes indicative of an integrated stress response (ISR). Experiment Overall Design: Mouse 3T3-L1 RNA for each time point was isolated from two control (LA) and two treatment (CLA) samples for analysis on four microarrays.

2008-06-16 | E-GEOD-8683 | biostudies-arrayexpress

Gene expression in 3T3-L1 mouse tissue (preadipocytes) treated with Trans-10,Cis-12 conjugated linoleic acid(t10c12 CLA)

2008-01-11 | GSE8683 | GEO

Detection of microRNA expression during 3T3-L1 pre-adipocyte differentiation using a custom made microarray chip.

Project description:Differentiation of 3T3-L1 cells into adipocytes involves a highly orchestrated series of events including clonal expansion, growth arrest and terminal differentiation. The mechanisms coordinating these different steps are not yet fully understood. Here we investigated whether micro (mi)RNAs play a role in this process. Microarray analysis was performed to detect miRNA expression during 3T3-L1 preadipocyte differentiation. Several miRNAs, including let-7, were up-regulated during 3T3-L1 adipogenesis. Ectopic introduction of let-7 into 3T3-L1 cells inhibited clonal expansion as well as terminal differentiation. The mRNA encoding high mobility group AT-hook 2 (HMGA2), a transcription factor that regulates growth and proliferation in other contexts, was inversely correlated with let-7 levels during 3T3-L1 cell adipogenesis, and let-7 markedly reduced HMGA2 concentrations. Knockdown of HMGA2 inhibited 3T3-L1 differentiation. These results suggest that let-7 plays an important role in adipocyte differentiation and that it does so in part by targeting HMGA2, thereby regulating the transition from clonal expansion to terminal differentiation.

2009-05-26 | GSE16229 | GEO

Detection of microRNA expression during 3T3-L1 pre-adipocyte differentiation using a custom made microarray chip.

2010-05-18 | E-GEOD-16229 | biostudies-arrayexpress

Multiple Roles for Steroid Receptor RNA Activator (SRA) in Regulation of Adipogenesis and Insulin Sensitivity

Project description:PPARM-NM-3 is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARM-NM-3 coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA Steroid receptor RNA Activator, SRA, associates with PPARM-NM-3 and coactivates PPARM-NM-3-dependent reporter gene expression. Overexpression of SRA in ST2 adipocyte precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes in cell cycle, insulin and TNFM-NM-1 signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARM-NM-3. SRA increases insulin-stimulated glucose uptake in adipocytes. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of cyclin-dependent kinase inhibiters p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the TNFM-NM-1-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways. Total RNA was isolated from fully differentiated (MDIT day 4) SRA overexpressing (pMSCV-SRA) and control (pMSCV empty vector) ST2 adipocytes, or fully differentiated (MDIT day 8) shSRA knockdown (pSuperior-shSRA) or shControl (pSuperior-shcontrol) 3T3-L1 adipocytes. Genome wide gene expression analysis was performed using Affymetrix mouse genome 430 2.0 arrays. Triplicate samples were analyzed.

2013-05-07 | E-GEOD-21594 | biostudies-arrayexpress

Glucocorticoid Signaling Defines a Novel Commitment State during Adipogenesis In Vitro

Project description:Differentiation of 3T3-L1 preadipocytes can be induced by a 2-d treatment with a factor "cocktail" (DIM) containing the synthetic glucocorticoid dexamethasone (dex), insulin, the phosphodiesterase inhibitor methylisobutylxanthine (IBMX) and fetal bovine serum (FBS). We temporally uncoupled the activities of the four DIM components and found that treatment with dex for 48 h followed by IBMX treatment for 48 h was sufficient for adipogenesis, whereas treatment with IBMX followed by dex failed to induce significant differentiation. Similar results were obtained with C3H10T1/2 and primary mesenchymal stem cells. The 3T3-L1 adipocytes differentiated by sequential treatment with dex and IBMX displayed insulin sensitivity equivalent to DIM adipocytes, but had lower sensitivity to isoproterenol-stimulated lipolysis and reduced triglyceride content. The nondifferentiating IBMX–then-dex treatment produced transient expression of adipogenic transcriptional regulatory factors C/EBP{beta} and C/EBP{delta}, and little induction of terminal differentiation factors C/EBP{alpha} and PPAR{gamma}. Moreover, the adipogenesis inhibitor preadipocyte factor-1 (Pref-1) was repressed by DIM or by dex-then-IBMX, but not by IBMX-then-dex treatment. We conclude that glucocorticoids drive preadipocytes to a novel intermediate cellular state, the dex-primed preadipocyte, during adipogenesis in cell culture, and that Pref-1 repression may be a cell fate determinant in preadipocytes.

2008-07-25 | GSE11249 | GEO

Expression data from mouse preadipocyte 3T3-L1 and slincRAD-shRNA-8 cells

Project description:Expression data from mouse preadipocyte 3T3-L1 and slincRAD-shRNA-8 cells

| PRJNA503332 | ENA

YG001: A Usp7-Tip60 pathway regulates early adipogenesis

Project description:USP7, a dominant DUB activity in 3T3-L1 adipocytes and in mouse adipose tissue, increases Tip60 protein levels, and deubiquitinates Tip60 both in intact cells and in vitro. Treatment with a pan deubiquitinase (DUB) inhibitor, or knockdown of USP7, decreases adipogenesis. Transcriptome analysis reveals a common set of cell cycle genes to be co-regulated by both Tip60 and USP7. Knock down of either factor results in impaired mitotic clonal expansion, an early step in adipogenesis. These results therefore reveal deubiquitination of a transcriptional coregulator to be a key mechanism in the regulation of early adipogenesis Mature 3T3-L1 adipocytes were subjected to RNAi-mediated knock down with control(C), USP7(U)- or Tip60(T)-specific oligonucleotides. For this, 4 replicates of differentiated 3T3-L1 cells were transfected with Amaxa technology. Two days after transfection cells were washed twice with PBS twice and lysed in 0.5ml Trizol (Invitrogen). mRNA expression of Tip60 and USP7 was assessed by qRT-PCR. Amplified cRNA samples were labeled with either cy3 or cy5 and put on microarray together with and oppositely labeled common reference sample consisting of cRNA derived from undifferentiated 3T3-L1 cells.

2013-08-28 | E-GEOD-28587 | biostudies-arrayexpress

Genome-wide RING1B binding in Fbxl10 overexpressing 3T3-L1 cells at day 2 of differentiation

Project description:We analyzed RING1B binding regions in 3T3-L1 cell lines transduced with the retroviral vector for V5-tagged Fbxl10 or its dF-box mutant. RING1B ChIP-seq in empty, Fbxl10-1, and dF-box mutant vector transduced 3T3-L1 preadipocytes, in duplicate, and V5-Fbxl10 ChIP-seq in Fbxl10 overexpressing 3T3-L1 cells

2015-03-04 | E-GEOD-64312 | biostudies-arrayexpress

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