Bacterial lipopolysaccharide-induced inflammation promotes iron accumulation in human adipocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE241167 | GEO | 2023/11/08
REPOSITORIES: GEO
Similar Datasets
Project description:Bacterial lipopolysaccharide-induced inflammation promotes iron accumulation in human adipocytes
| PRJNA1006670 | ENA
Project description:Recents studies in mice and humans demonstrated the relevance of H2S-synthesising enzymes (such as CTH, CBS and MPST) in adipose tissue physiology and preadipocyte differentiation into adipocytes. Here, we aimed to investigate the combined role of CTH, CBS and MPST in the preservation of adipocyte protein persulfidation and adipogenesis. Joint CTH, CBS and MPST gene knockdown was achieved treating fully human adipocytes with siRNAs against these transcripts (siRNA_MIX). Adipocyte protein persulfidation was analyzed by a mass spectrometry label-free quantitative approach coupled with a dimedone-switch method for protein labeling and purification. The proteomic analysis quantified 216 proteins with statistically different persulfidation levels in KD cells compared to control adipocytes. In fully differentiated adipocytes, CBS and MPST mRNA and protein levels were abundant, whereas CTH expression was very low. Of note, siRNA_MIX administration resulted in a significant decrease in CBS and MPST expression, without impacting on CTH. Dual CBS and MPST gene knockdown resulted in decreased expression of relevant genes for adipocyte biology, including adipogenesis, mitochondrial biogenesis and lipogenesis, but increased proinflammatory- and senescence-related genes, in parallel to a significant disruption in adipocyte protein persulfidation pattern. While among less persulfidated proteins, we identified several relevant proteins for adipocyte adipogenesis and function, among the most persulfidated, key mediators of adipocyte inflammation and dysfunction, but also some proteins that might have a positive role of adipogenesis were found. In conclusion, current study indicates that joint knockdown of CBS and MPST (but not CTH) in adipocytes impairs adipogenesis and promotes inflammation, possibly by disrupting the pattern of protein persulfidation in these cells, and suggesting that these enzymes were required for the functional maintenance of adipocytes.
2022-08-12 | PXD032370 | Pride
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
Project description:The mechanisms promoting disturbed white adipocyte function in obesity remain largely unclear. Herein, we integrate white adipose tissue (WAT) metabolomic and transcriptomic data from clinical cohorts and find that the WAT phosphocreatine/creatine ratio is increased and creatine kinase-B expression and activity is decreased in the obese state. . In human in vitro and murine in vivo models, we demonstrate that decreased phosphocreatine metabolism in white adipocytes alters AMPK activity via effects on ATP/ADP levels, independently of WAT beigeing. This disturbance promotes a pro-inflammatory profile characterized, in part, by increased CCL2 production. These data suggest that the phosphocreatine/creatine system links cellular energy shuttling with pro-inflammatory responses in human and murine white adipocytes. Our findings provide unexpected perspectives on the mechanisms driving WAT inflammation in obesity and may present avenues to target adipocyte dysfunction.
2022-01-27 | GSE192361 | GEO
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.
2010-01-08 | GSE19757 | GEO
Project description:Obesity is considered an important factor for many chronic diseases, including diabetes, cardiovascular disease and cancer. The expansion of adipose tissue in obesity is due to an increase in both adipocyte progenitor differentiation and mature adipocyte cell size. Adipocytes, however, are thought to be unable to divide or enter cell cycle. We demonstrate that mature human adipocytes unexpectedly display a gene and protein signature of cell cycle re-entry. Adipocyte cell cycle progression associates with obesity and hyperinsulinemia, with a concomitant increase in cell size, nuclear size and nuclear DNA content. However, chronic hyperinsulinemia in vitro or in patients, is associated with subsequent cell cycle exit, leading to a premature senescent transcriptomic and secretory profile in adipocytes. Premature senescence is rapidly becoming recognized as an important mediator of stress-induced tissue dysfunction. By demonstrating that adipocytes can re-enter cell cycle we define a mechanism for how mature, human adipocytes senesce and demonstrate that by targeting the adipocyte cell cycle program it is possible to impact adipocyte senescence and obesity-associated adipose tissue inflammation.
| EGAS00001005770 | EGA
Project description:Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes. We used microarrays to examine gene expression in differentiated pre-adipocytes treated with and without an SCD inhibitor. On day 7 of adipocyte differentiation, total RNA was extracted from adipocytes. Two conditions were selected for comparison: total RNA extracted from adipocytes treated with DMSO (control) and or a SCD inhibitor.
2014-04-04 | E-GEOD-51905 | biostudies-arrayexpress
Project description:Genome-wide DNA methylation profiling was performed of human mesenchymal stem cells (hMSCs) differentiating into adipocytes (day 10). The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to measure DNA methylation of hMSC before differentiation (day 0) and of adipocytes at day 10 of differentiation. Our aims were to 1) measure genome-wide DNA methylation changes during adipocyte differentiation in primary hMSCs and 2) investigate the relationship between DNA methylation and gene expression regulation in a panel of 84 adipocyte-related genes. Bisulphite converted DNA from four independent experiments was hybridised to the Illumina Infinium 450k Human Methylation Beadchip. The first comparison was made between undifferentiated hMSCs and differentiated adipocytes at day 10. As a positive control, differentiating cells were continuously exposed to 5-Aza-2â²-deoxycytidine (5-aza-dC). The second comparison was made between differentiated adipocytes at day 10 and 5-aza-dC exposed adipocytes at day 10.
2016-04-13 | E-GEOD-74609 | biostudies-arrayexpress
Project description:Brown adipose tissue is specialized to burn lipids for heat generation as a natural defense against cold and obesity. Previous studies established microRNAs as essential regulators of brown adipocyte differentiation, but it remains unknown whether microRNAs are required for the feature maintenance of mature brown adipocytes. To address this question, we ablated Dgcr8, a key regulator of the microRNA biogenesis pathway, in mature brown as well as white adipocytes. The adipose tissue -specific Dgcr8 knockout mice displayed enlarged but pale interscapular brown fat with decreased expression of genes characteristic of brown fat, and the mice were intolerant to cold exposure. In vitro primary brown adipocyte cultures confirmed that microRNAs are required for marker gene expression in mature brown adipocytes. We also demonstrated that microRNAs are essential for the browning of subcutaneous white adipocyte both in vitro and in vivo. Using this animal model, we performed microRNA expression profiling analysis and identified a set of BAT-specific microRNAs that are up-regulated during brown adipocyte differentiation and enriched in brown fat compared to other organs. We identified miR-182 and miR-203 as new regulators of brown adipocyte development. Taken together, our study demonstrates an essential role of microRNAs in the maintenance as well as the differentiation of brown adipocytes. TotalRNAs were extracted using a Qiagen kit, and 5 M-NM-<g of total RNAs for each sample were used to prepare the mRNA- Seq library according to the manufacturerM-bM-^@M-^Ys instruction (NEB). cDNA libraries were prepared and sequenced by Hi-seq in Whitehead Genome Core. 2 replicates of each treatment were analyzed.
2014-08-07 | E-GEOD-60165 | biostudies-arrayexpress
Project description:Genome-wide DNA methylation profiling was performed of human mesenchymal stem cells (hMSCs) differentiating into adipocytes (day 10). The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to measure DNA methylation of hMSC before differentiation (day 0) and of adipocytes at day 10 of differentiation. Our aims were to 1) measure genome-wide DNA methylation changes during adipocyte differentiation in primary hMSCs and 2) investigate the relationship between DNA methylation and gene expression regulation in a panel of 84 adipocyte-related genes.
2016-04-13 | GSE74609 | GEO