Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adipocytes alter the ALL translational programme to enhance their dormancy and stress resistance.

ABSTRACT: We investigated the possibility that adipocyte mediated stress protection is accompanied by activation of a selective mRNA translation analogous to stress induced translational arrest. Nalm-6 cells were subjected at +24 and +48h under 3T3-L1 adipocyte co-culture to Pulsed Stable Isotope Chromatography-mass spectrometry (SILAC) based proteomic analysis to estimate protein translation rates over time relative to pre-adipocyte control conditions.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Cell, Cell Culture

DISEASE(S): Acute Leukemia

SUBMITTER: Faraz Mardakheh

LAB HEAD: Faraz Mardakheh

PROVIDER: PXD019369 | Pride | 2021-06-11

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Similar Datasets

Adipose MDM2 regulates systemic insulin sensitivity through nuclear import of MORC2 and the PPARγ cofactor LIPIN1

Project description:The intimate association between obesity and type II diabetes urges for a deeper understanding of adipocyte function. We and others have previously delineated a role for the tumor suppressor p53 in adipocyte biology. Here, we show that mice haploinsufficient for MDM2, a key regulator of p53, in their adipose stores suffer from overt obesity, insulin resistance, and hepatic steatosis. These mice had decreased levels of circulating palmitoleic acid (non-esterified fatty acid (NEFA) 16:1) concomitant with impaired visceral adipose tissue expression of Scd1 and Ffar4. A similar decrease in Scd and Ffar4 expression was found in in vitro differentiated adipocytes with perturbed MDM2 expression. Mechanistically, lowered MDM2 levels led to nuclear exclusion of the transcriptional cofactors, MORC2 and LIPIN1, thus hampering adipocyte function by antagonizing LIPIN1-mediated PPARγ coactivation. Collectively, these data argue for a p53-independent role of MDM2 in controlling adipocyte function through LIPIN1.

2022-02-15 | PXD020812 | Pride

Browning of human adipocytes requires KLF11 and reprogramming of PPARγ super-enhancers

Project description:Here we have characterized the transcriptional processes underlying the formation of human brown in white (i.e. brite) adipocytes using a genome-wide approach. We show that the browning process is associated with reprogramming of peroxisome proliferator-activated receptor γ (PPARγ) binding to form brite adipocyte-selective PPARγ super-enhancers that appear to play a key role in activation of brite adipocyte-selective genes. We identify the KLF11 gene based on its association with a PPARγ super-enhancer and show that KLF11 is a novel browning factor directly induced by rosiglitazone and required for the activation of brite adipocyte-selective gene program by rosiglitazone. Genome-wide profiling of Dnase I hypersenstive (DHS) sites, epigenomic marks, transcription factor and co-factor binding, and gene expression in hMADS white and brite adipocytes

2014-12-12 | E-GEOD-59703 | biostudies-arrayexpress

Adipocytes disrupt the translational programme of Acute Lymphoblastic Leukaemia to favour tumour survival and persistence

Project description:Nalm-6 cells co-cultured with 3T3-L1 adipocytes or pre-adipocytes were subjected to quantitative LC-MS/MS phosphoproteomic analysis at two timepoints (+24h and +72h) to determine dynamics of cell signalling. Two independent biological replicates were analysed per condition.

2021-06-09 | PXD019186 | Pride

iTRAQ-Based Quantitative Proteomic Comparison of 2D and 3D Adipocyte Cell Models Co-cultured with Macrophages Using Online 2D-nanoLC-ESI-MS/MS

Project description:The demand for novel three-dimensional (3D) cell culture models of adipose tissue has been increasing, and proteomic investigations are important for determining the underlying causes of obesity, type II diabetes, and metabolic disorders. In this study, we performed global quantitative proteomic profiling of three 3D-cultured 3T3-L1 cells (preadipocytes, adipocytes and co-cultured adipocytes with macrophages) and their 2D-cultured counterparts using 2D-nanoLC-ESI-MS/MS with iTRAQ labelling. A total of 2,885 shared proteins from six types of adipose cells were identified and quantified in four replicates. Using iTRAQ-based quantitative assessments, we found that the primary proteins involved in carbohydrate and fatty acid metabolism, adipogenesis and the electron transport chain were highly expressed in 3D cell culture system when compared to those of 2D-cultured cells. Furthermore, it was also shown that the expression levels of proteins associated with metabolic pathways, carbon metabolism and glycolysis/gluconeogenesis were up-regulated, whereas proteins implicated in both DNA replication and the cell cycle were expressed at lower levels compared to those of the 2D mono-cultured cells. Based on these results, the 3D adipocyte model can help elucidate the mechanisms underpinning metabolic syndromes and aid the development of new medical treatments for metabolic disorders.

2020-05-26 | PXD014437 | Pride

Calorie restriction-induced changes in the secretome of human adipocytes, comparison with resveratrol-induced secretome effects

Project description:Obesity is characterized by excess energy storage which results in dysfunctional white adipose tissue (WAT) and in turn leads to metabolic diseases. Lifestyle changes especially calorie restriction (CR) reduces the risk for age and obesity-associated complications. The impact of CR on obesity has mainly been examined with human intervention studies, which indicated alterations in circulating adipokines. However, a detailed understanding of CR-induced adipocyte secretome changes remains elusive. Therefore, we investigated the effect of CR on the secretion profile of mature human adipocytes by using proteomics technology with bioinformatic analysis. We demonstrated CR-mediated adipocyte triglyceride reduction, which resulted in a positive effect on adipokine secretion indicating an improved inflammatory phenotype and alleviation of obesity-associated metabolic dysfunction including insulin resistance and glucose intolerance. Furthermore, 6 novel adipocyte-secreted proteins were identified which were regulated by CR. Since resveratrol (RSV) mimics CR we compared results from this study with data from our previous RSV study on the adipocyte secretome. We observed that both treatment strategies lead to a less inflammatory phenotype and an altered adipokine profile indicating improvement of metabolic complications even though the CR and RSV adipocyte secretomes differed from each other.

2016-05-25 | PXD000301 | Pride

Comparative proteomic profiling of 3T3-L1 adipocyte differentiation using SILAC quantification

Project description:Comparative proteomic profiling of 3T3-L1 adipocyte differentiation using SILAC quantification

2020-10-26 | PXD019716 | Pride

Adipocyte vesicles: ‘all-in-one’ packages that stimulate tumor mitochondrial metabolism and dynamics

Project description:Extracellular vesicles are emerging key actors in adipocyte communication. Notably, small extracellular vesicles shed by adipocytes promote melanoma aggressiveness through fatty acid oxidation, with a heightened effect in obesity. However, the vesicular actors and cellular processes involved remain largely unknown. Here, we elucidate the mechanisms linking adipocyte extracellular vesicles to metabolic remodeling and cell migration. Using an adapted SILAC technique, we show that adipocyte vesicles stimulate melanoma fatty acid oxidation by providing both enzymes and substrates. In obesity, the heightened effect of extracellular vesicles depends on increased transport of fatty acids, not fatty acid oxidation related enzymes as shown by classical LC-MS/MS analysis. These fatty acids, stored within lipid droplets in cancer cells, drive fatty acid oxidation after release through lipophagy. This increase in mitochondrial activity redistributes mitochondria to membrane protrusions of migrating cells, which is necessary to increase cell migration in the presence of adipocyte vesicles. Our results provide key insights into the role of extracellular vesicles in the metabolic cooperation that takes place between adipocytes and tumors with particular relevance in obesity.

2020-01-09 | PXD014487 | Pride

Expression Data from Bone Marrow Progenitor-Derived Adipocytes, White Adipocytes and Brown Adipocytes.

Project description:We have identified a population of adipocytes in fat tissue that arise from bone marrow-derived progenitor cells. We used microarrays to compare the global gene expression patterns of the bone marrow progenitor-derived adipocytes as well as conventional white and brown adipocytes to evaluate the relationship between these adipocyte subpopulations. Gonadal fat tissue (for white adipocytes) and intrascapular fat tissue (for brown adipocytes) was digested with collagenase and adipocytes were recovered by centrifugation/flotation. Bone marrow derived adipocytes were isolated from the adipocyte fraction of gonadal fat tissue from mice receiving bone marrow tranplants from donors expressing either green fluorescent protein (GFP) or beta-galactosidase (LacZ) by flow cytometry.

2010-01-08 | E-GEOD-19757 | biostudies-arrayexpress

Folate and vitamin B12 imbalance induces endoplasmic reticulum stress and cholesterol biosynthesis gene expression in human adipocytes

Project description:Rationale: Low B12 has been shown to play an important role in the prediction of metabolic risk, but its significance and mechanism in the development of adiposity and adipose tissue dysfunction is largely unknown. Objective: To investigate the role of B12 and folic acid in the development of adipocyte dysfunction. Methods and Results: Microarray analysis of human adipocytes (CHUB-S7 cell line) cultured and differentiated in customised media with varying concentrations of B12 and folic acid led to the identification of two important pathways: cholesterol synthesis and unfolded protein response (UPR). Adipocytes cultured in media with low B12 (150 pmol/L) or no B12 had increased intracellular total cholesterol, higher secreted homocysteine levels, induced UPR and reduced glucose uptake capacity compared to adipocytes cultured in normal media with higher B12. The folate concentrations had either no or little effect on the measured functions. Further analysis of these adipocytes for overall DNA methylation showed that the promoter regions of sterol regulatory element-binding transcription factor 1 (SREBF1) and low density lipoprotein receptor (LDLR) were hypomethylated in the low and no B12 conditions. The SREB proteins (SREBP1 and 2) and mRNA expressions (SREBF1 and LDLR) were also increased in the same conditions. Conclusion: The data suggest that low B12 can lead to adipocyte dysfunction by inducing excess cholesterol biosynthesis, homocysteine production and induction of UPR and overall adipocyte dysfunction. Both of these pathways and adipocyte dysfunction play a significant role in the development of cardiovascular diseases. Independent replicate samples of the human adipocyte cell line CHUB-S7 were treated with four different concentrations of B12 and folate.

2012-12-30 | E-GEOD-43166 | biostudies-arrayexpress

Long non-coding RNAs regulate adipogenesis (Illumina RNA-Seq)

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data