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Expression data from SGBS human cells before and after 24 hours of stimulation with differentiation cocktail, with or without Scrambled (Scr) or Tenomodulin (TNMD) siRNA to knockdown the genes of interest.

ABSTRACT: In a screen for upregulated adipocyte genes in insulin resistant versus insulin sensitive subjects matched for BMI, we identified the type II transmembrane protein tenomodulin (TNMD), previously implicated in glucose tolerance in gene association studies. TNMD expression was greatly increased in human preadipocytes during differentiation, while silencing TNMD blocked adipogenic gene induction and adipogenesis. We used microarrays to identify genes of interest that are differentially expressed after the addition of siRNA to tenomodulin or scrambled siRNA, in both preadipocytes and partially differentiated adipocytes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76319 | GEO | 2016/02/11

SECONDARY ACCESSION(S): PRJNA306888

REPOSITORIES: GEO

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Expression data from SGBS human cells before and after 24 hours of stimulation with differentiation cocktail, with or without Scrambled (Scr) or Tenomodulin (TNMD) siRNA to knockdown the genes of interest.

Project description:In a screen for upregulated adipocyte genes in insulin resistant versus insulin sensitive subjects matched for BMI, we identified the type II transmembrane protein tenomodulin (TNMD), previously implicated in glucose tolerance in gene association studies. TNMD expression was greatly increased in human preadipocytes during differentiation, while silencing TNMD blocked adipogenic gene induction and adipogenesis. We used microarrays to identify genes of interest that are differentially expressed after the addition of siRNA to tenomodulin or scrambled siRNA, in both preadipocytes and partially differentiated adipocytes. SGBS preadipocytes were treated with scrambled or siTNMD. Cells either were kept undifferentiated or stimulated for 24 hours with differentiation cocktail. Cells were prepared with this protocol on three different occasions and total RNA was isolated to provide three biological replicates per sample.

2016-02-11 | E-GEOD-76319 | biostudies-arrayexpress

Proteomic characterization of SGBS cells

Project description:In this study, SGBS preadipocytes were differentiated for 12 days into mature preadipocytes.

2021-09-16 | PXD023266 | Pride

Preadipocytes of T2DM patients display an intrinsic gene expression profile of decreased differentiation capacity

Project description:Insulin resistance and Type 2 Diabetes Mellitus (T2DM) are associated with increased adipocyte size, altered secretory pattern and decreased differentiation of preadipocytes. To identify the underlying molecular processes in preadipocytes of T2DM patients that are a characteristic of the development of T2DM, preadipocyte cell cultures were prepared from subcutaneous fat biopsies of T2DM patients and compared with age- and BMI matched control subjects. Gene expression profiling showed changed expression of transcription factors involved in adipogenesis and in extracellular matrix remodeling, actin cytoskeleton and integrin signaling genes, which indicated decreased capacity to differentiate. Additionally, genes involved in insulin signaling and lipid metabolism were down-regulated, and inflammation/apoptosis was up-regulated in T2DM preadipocytes. The down-regulation of genes involved in differentiation can provide a molecular basis for the reduced adipogenesis of preadipocytes of T2DM subjects, leading to reduced formation of adipocytes in subcutaneous fat depots, and ultimately leading to ectopic fat storage. 7 T2DM preadipocyte samples and 9 age- and BMI-matched control samples were hybridized using 70-mer oligonucleotide microarrays. Samples were labeled with either Cy3 or Cy5. A total of 20 arrays were used including dye swop. Per array, a T2DM sample was hybridized with a control sample of the same gender and matched based on age and BMI. To ensure hybridization of two samples with the same gender, three T2DM (5064, 5128, 5395) and one control sample (5616) were used twice and listed as technical replicates.

2010-05-16 | E-GEOD-15790 | biostudies-arrayexpress

Preadipocytes of T2DM patients display an intrinsic gene expression profile of decreased differentiation capacity

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Increased body mass index is linked to systemic inflammation through altered chromatin co-accessibility in human preadipocytes [RNA-Seq]

Project description:Obesity-induced adipose tissue dysfunction can cause low-grade inflammation and downstream obesity comorbidities. Although preadipocytes may contribute to this pro-inflammatory environment, the underlying mechanisms are unclear. We used human primary preadipocytes from body mass index (BMI) -discordant monozygotic (MZ) twin pairs to generate epigenetic (ATAC-sequence) and transcriptomic (RNA-sequence) data for testing whether increased BMI alters the subnuclear compartmentalization of open chromatin in the twins’ preadipocytes, causing downstream inflammation. Here we show that the co-accessibility of open chromatin, i.e. compartmentalization of chromatin activity, is altered in the higher vs lower BMI MZ siblings for a large subset (~88.5Mb) of the active subnuclear compartments. Using the UK Biobank we show that variants within these regions contribute to systemic inflammation through interactions with BMI on C-reactive protein. In summary, open chromatin co-accessibility in human preadipocytes is disrupted among the higher BMI siblings, suggesting a mechanism how obesity may lead to inflammation via gene-environment interactions.

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Increased body mass index is linked to systemic inflammation through altered chromatin co-accessibility in human preadipocytes [ATAC-Seq]

2023-06-28 | GSE235361 | GEO

LSD1 knockdown in 3T3-L1 preadipocytes

Project description:Obesity is often associated with a low-grade systemic inflammation state that contributes to the development of insulin resistance and atherosclerotic complications. This is usually coupled with increased macrophage infiltration in the adipose tissue and a defect in adipocyte differentiation that results in accumulation of hypertrophic fat cells characterized by a deregulated pattern of adipokine expression. Here we show that knockdown of histone demethylase lsd1 in 3T3-L1 preadipocytes results in defective adipogenesis and derepression of an inflammatory program in these cells. The dataset consists of four sample groups: [1] 3T3-L1 preadipocytes (passage 19) transfected with a control scrambled siRNA at 24h after transfection (siC.24h), [2] 3T3-L1 preadipocytes (p.19) transfected with a siRNA directed against LSD1 at 24h after transfection (siLsd1.24h), [3] 3T3-L1 preadipocytes (p.21) transfected with a control scrambled siRNA at 48h after transfection (siC.48h), and [4] 3T3-L1 preadipocytes (p.21) transfected with a siRNA directed against LSD1 at 48h after transfection (siLsd1.48h). The 24h sample groups (siC.24h and siLsd1.24h) consist of two biological replicate samples; the 48h sample groups (siC.48h and siLsd1.48h) consist of three biological replicate samples. Each sample was hybridized to a separate array, for a total of ten arrays.

2013-12-31 | E-GEOD-25423 | biostudies-arrayexpress

Adverse Effects of Bisphenol A and its substitute compounds on human SGBS preadipocytes

Project description:Bisphenol A (BPA), which is used in a variety of consumer-related plastic products, was reported to cause metabolic disruption. Substitute compounds are increasingly emerging, but are not sufficiently investigated. In this study, we aimed to investigate the mode of action of BPA and four of its substitutes during the differentiation of human preadipocytes. Human preadipocytes were exposed to BPA, BPS, BPB, BPF, and BPAF, as well as the PPARγ-antagonist GW9662. After 12 days of differentiation, global protein profiles were assessed using LC-MS/MS-based proteomics.

2021-08-05 | PXD023227 | Pride

Insulin resistance rewires the metabolic gene program and glucose utilization in human white adipocytes

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Genetic Risk Factors for Type 2 Diabetes: A Trans-Regulatory Genetic Architecture?

Project description:Transcriptional Profiling of Insulin Sensitive and Insulin Resistant Samples Sixty two participants at the tail ends of the distribution of insulin sensitivity adjusted for age, gender and natural logarithm of BMI for each ethnic group separately. Individuals at tail ends were well matched for age, gender, BMI, and percent fat, but were different for insulin sensitivity. Participants were of age 20 years to 55 years, body mass index (BMI) between 19 kg/m2 and 42 kg/m2, and had all biopsies obtained in the fasting state.

2013-04-16 | E-GEOD-40234 | biostudies-arrayexpress

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