3T3-L1
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Tae Youl Ha
PROVIDER: E-MTAB-1783 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Objective: Potential regulators of adipogenesis include microRNAs (miRNAs), small non-coding RNAs that have been recently shown related to adiposity and differentially expressed in fat depots. However, to date no study is available regarding the relationship of miRNAs expression profile, biological pathway and cellular phenotype during human adipogenesis. Thereby, the aim of this study was to investigate whether miRNA expression profile in human adipocytes is related to adipogenesis and to test whether miRNA profile in human subcutaneous adipose tissue is associated to human obesity and co-morbidities. Keywords: miRNA expression Three biological replicates of fat cells from both lean (BMI<25.0Kg/m2) and obese (BMI>30.0Kg/m2) subjects during differentiation (days 0, 7 and 14) were performed.
2010-05-13 | E-GEOD-18469 | biostudies-arrayexpress
Project description:Human abdominal adipose tissue was obtained with informed consent from a 33-year old Caucasian female (BMI = 32.96 Kg/m2) undergoing lipoaspiration. Adipose stromal cells (hASCs) were isolated and differentiated into adipocytes in vitro. Two technical replicates from 9 time points relative to induction of adipogenesis (day 0). Also, one sample from pre-adipocytes (day -2) grown without FGF.
2010-09-30 | E-GEOD-20699 | biostudies-arrayexpress
Project description:Obesity has become a global health problem. Brown adipose tissue (BAT), specialized for energy expenditure through thermogenesis, potently counteracts obesity. Recently, BAT is also identified in human adults. We found that Lgr4 homozygous mutant (Lgr4m/m) mice display reduced adiposity and exhibit brown-like adipocytes in their WAT depots with higher expression of uncoupling protein 1 (Ucp1). Furthermore, Lgr4 ablation potentiates brown adipocyte differentiation from stromal vascular fraction (SVF) of epididymal WAT (eWAT) in vitro. We used microarrays to emxamine the gene expression profiles of the brown-like adipocytes differentiated from SVF of wild-type and Lgr4 mutant mice. We identified distinct gene expression profiles of these two groups. To demonstrate Lgr4 ablation can potentiate the differentiation of SVF from eWAT toward brown-like adipocytes in vitro, we isolated SVF from epididymal white adipose tissue (eWAT) of wild-type (WT) and Lgr4 mutant mice. We then plated SVF cells in 12-well plate, and differentiated them to brown adipocytes, followed by RNA extraction and hybridization with Affymetrix microarrays.
2013-11-07 | E-GEOD-47760 | biostudies-arrayexpress
Project description:Human abdominal adipose tissue was obtained with informed consent from a 33-year old Caucasian female (BMI = 32.96 Kg/m2) undergoing lipoaspiration. Adipose stromal cells (hASCs) were isolated and differentiated into adipocytes in vitro. Two technical replicates from 9 time points realtive to induction of adipogenesis (day 0). Also, two technical replicated from pre-adipocytes (day -2) grown without FGF. Two individual replicates (day 1 and day 7) were removed due to failed hybridizations.
2010-09-30 | E-GEOD-20697 | biostudies-arrayexpress
Project description:Adipogenesis is a physiological process required for fat-tissue development, mainly involved in regulating the organism energetic-state. Abnormal distribution-changes and dysfunctions in such tissue are associated to different pathologies. Adipocytes are generated from progenitor cells, via a complex differentiating process not yet well understood. Therefore, we investigated differential mRNA and miRNA expression patterns of human mesenchymal stromal-cells (MSC) induced and not induced to differentiate into adipocytes by next (second)-generation sequencing. A total of 2,866 differentially-expressed genes (101 encoding miRNA) were identified, with 705 (46 encoding miRNA) being upregulated in adipogenesis. They were related to different pathways, including PPARG, lipid, carbohydrate and energy metabolism, redox, membrane-organelle biosynthesis and endocrine system. Downregulated genes were related to extracellular matrix and cell migration, proliferation and differentiation. Analyses of mRNA-miRNA interaction showed that repressed miRNA-encoding genes can act downregulating PPARG-related genes; mostly the PPARG activator (PPARGC1A). Induced miRNA-encoding genes regulate downregulated genes related to TGFB1. These results shed new light to understand adipose-tissue differentiation and physiology, increasing our knowledge about pathologies like obesity, type-2 diabetes and osteoporosis.
2016-08-31 | E-MTAB-4884 | biostudies-arrayexpress
Project description:Brown adipocytes are specialized for heat generation and energy expenditure as a defense against cold and obesity. Recent studies demonstrate that brown adipocytes arise in vivo from a Myf5-positive, myoblastic progenitor by the action of PRDM16. Here, we identified a brown fat-enriched miRNA cluster mir-193b-365 as a key regulator of brown fat development. Blocking miR-193b and/or miR-365 in primary brown preadipocytes dramatically impaired brown adipocyte adipogenesis whereas myogenic markers were significantly induced. Forced expression of miR-193b and/or miR-365 in C2C12 myoblasts blocked the entire program of myogenesis, and miR-193b induced myoblasts to differentiate into brown adipocytes. Mir-193b-365 was upregulated by PRDM16. Our results demonstrate that mir-193b-365 serves as an essential regulator for brown fat differentiation, in part by repressing myogenesis. To study if miR-193b-365 is required for brown adipocyte adipogenesis, mRNAs from cultured primary brown adipocytes (Day 4) transfected with each locked nucleic acid (LNA) miRNA inhibitor or Control inhibitor were analyzed by microarray analysis.
2011-05-02 | E-GEOD-27614 | biostudies-arrayexpress
Project description:Adipogenesis involves the regulation of hundreds of genes by several well-studied proteins, but the role of long, noncoding RNAs in this process has not been defined. We track the regulation of hundreds of lncRNAs during adipocyte differentiation, and find several that are essential for this process. We extractedbrown and white primary adipocytes and pre-adipocytes and profiled lncRNA expresssion via mRNA-Seq. We also profiled cultured, differentiated adipocytes to verify that we could recapitulate the adipocyte expression profile in preparation for a loss-of-function screen for essential adipogenic lincRNAs.
2013-02-15 | E-GEOD-29898 | biostudies-arrayexpress
Project description:Background: Exposure to the endocrine-disrupting chemical bisphenol A (BPA) is correlated with obesity and promotes adipogenesis of human preadipocytes into mature adipocytes. However, the mechanism of action of BPA-induced human adipogenesis in vitro remains to be fully characterized. Methods: In this study, potential mechanisms of BPA-induced adipogenesis in primary human preadipocytes were evaluated using gene expression microarray analysis. Preadipocytes from donors with normal body mass indexes were differentiated in the presence of 50 M-BM-5M BPA or 1 M-BM-5M dexamethasone (DEX) for 48 hours. Results: Microarray analysis revealed 235 up-regulated and 138 down-regulated genes following BPA treatment, including sterol regulatory element binding factor 1 (SREBF1), a key transcription factor known to regulate many components of lipid metabolism and adipogenesis. For DEX treated preadipocytes, 1136 genes were up-regulated, including the adipogenic marker lipoprotein lipase, while 1031 genes were down-regulated. Ingenuity Pathway Analysis was used to identify functional annotations of the gene expression changes associated with response to BPA and DEX treatments. BPA exposure was associated with expression changes in the genes involved in the accumulation of triacylglycerol while DEX was linked to metabolism of triacylglycerol and cleavage of fatty acids. The analysis also revealed enrichment of genes in pathways known to be associated with BPA exposure including thyroid-receptor/retinoic X receptor (TR/RXR) activation, mammalian target of rapamycin (mTOR) signaling and cholesterol biosynthesis, whereas DEX treatment was linked to cholesterol biosynthesis and ethanol degradation. Interestingly, alterations in the mTOR pathway in response to BPA did not occur in DEX-treated preadipocytes. Conclusions: Our data suggest that potential mechanisms of action of BPA-induced adipogenesis involve SREBF1, the TR/RXR and the mTOR pathways. The study used 40 samples in total which included 5 replicates (cells from 5 unique donors) of 8 different treatments. The 8 treatments were as follows: 1) untreated (negative) control for 48 hours, 2) 25 uM BPA treated for 48 hours, 3) 50 uM BPA treated for 48 hours, 4) untreated (negative) control + insulin for 48 hours, 5) 25 uM BPA + insulin treated for 48 hours, 6) 50 uM BPA + insulin treated for 48 hours, 7) 1uM Dexamethasone + insulin treated for 48 hours, 8) 1uM Dexamethasone + insulin treated for 96 hours.
2014-04-15 | E-GEOD-56085 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE27912: Gene-chip studies of adipogenesis-regulated microRNAs in mouse primary adipocytes and human obesity (Exiqon) GSE27949: Gene-chip studies of adipogenesis-regulated microRNAs in mouse primary adipocytes and human obesity (Affymetrix) Refer to individual Series
2011-06-10 | E-GEOD-27951 | biostudies-arrayexpress
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. 3T3-L1 cells were induced to differentiation into mature adipocytes using a canonical DMI cocktail. The time point at two days after confluency of 3T3-L1 was defined as day 0. Samples were collected at day 0, day 1, day 4, and day 7. The expression of microRNAs at day 1, day 4, and day 7 was compared to that of day 0.
2010-05-18 | E-GEOD-16229 | biostudies-arrayexpress