Genome wide methylation of subcutaneous adipose tissue collected from women with polycystic ovary syndrome (PCOS) and healthy controls.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Michelle Jones
PROVIDER: E-MTAB-3777 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Subcutaneous adipose tissue was collected from 23 PCOS cases and 13 healthy controls, and snap frozen in LN2 at collection. DNA and RNA was extracted and stored. Gene expression arrays were run in all samples.
2015-09-01 | E-MTAB-3768 | biostudies-arrayexpress
Project description:Suboptimal intrauterine nutrition predisposes the fetus to central obesity and metabolic syndrome in adult life, suggesting nutritional programming of the fat distribution. However, the underlying mechanisms are not elucidated. We hypothesized that prenatal nutritional deprivation leads to stimulation of adipogenesis, as an adaptive mechanism, in a depot-dependent manner. The induction of adipogenesis is most enhanced in the subcutaneous lower-body depots, followed by the subcutaneous upper-body and visceral adipose tissue depots. Stimulation of adipogenesis may lead to an early consumption of the stem cell pool, and thus, may impair adipose tissue expandability postnatally, which may lead to differences in regional adipose tissue growth. We tested this hypothesis by analyzing global gene expression to identify expression patterns in subcutaneous abdominal, subcutaneous femoral, and omental adipose depots of baboon fetuses that have been altered by nutritional maternal deprivation. Adipose tissue was collected from baboon fetuses at 165 dG from mothers fed control or 30% nutrient-restricted diets (three females and one male in each group). 24 samples, each consisted of pooled total RNA from triplicate wells (6-well plate).
2011-12-16 | E-GEOD-34464 | biostudies-arrayexpress
Project description:The aim of the project was to compare global gene expression in adipocytes from obese patients and lean controls. Subcutaneous adipose tissue was collected from severely obese patients undergoing bariatric surgery (average body-mass index (BMI) of 45.5 kg/m2 (n = 12, thereof 4 men) and healthy lean patients undergoing hernia repairs (average BMI of 24.2 kg/m2 (n = 12, thereof 7 men), between 27 and 56 years of age. Adipocytes were isolated by collagenase treatment of adipose tissue, followed by filtering and centrifugation. Floating adipocytes were lysed in Qiazol before RNA purification and microarray analysis.
2018-12-12 | E-MTAB-6728 | biostudies-arrayexpress
Project description:Obesity is a known risk factor for breast cancer. To identify genes and underlying pathways in human triple-negative breast cancer cells affected by interaction with adipose tissue, MDA-MB-231 breast cancer cells were cultivated in a co-culture system with or without adipose tissue explants from mice for the purpose of a microarray gene expression analysis. Co-culture of MDA-MB-231 breast cancer cells was performed with adipose tissue explants obtained from C57BL/6J mice that were fed a high-fat diet (HFD, 58%Kcal from fat) or normal chow diet (NC; 11%Kcal from fat) ad libitum for 16 weeks. For co-cultivation analyses of breast cancer cells and adipose tissue explants, we set up a two-dimensional transwell system, which enables intercellular communication through soluble factors secreted into the medium but inhibits intermixture of the different cell types. Following 72 hours of co-culture with or without adipose tissue, total RNA was isolated from the breast cancer cells and subjected to microarray gene expression analyses.
2020-08-17 | E-MTAB-9485 | biostudies-arrayexpress
Project description:Genome wide DNA methylation in blood, subcutaneous and omental visceral adipose tissue from two-step surgical approach (N=9) was analysed in patients with severe obesity using Illumina 850K EPIC technology before and after metabolic surgery (Leipzig Obesity BioBank (LOBB) cohort). Additionally, a validation blood cohort of patients with obesity undergoing metabolic surgery was analyzed for results validation.
2024-03-31 | E-MTAB-13564 | biostudies-arrayexpress
Project description:Methylation profiling of IDH WT, IDH1 and IDH2 mutated chondrosarcoma tumour samples
2022-03-01 | E-MTAB-11031 | biostudies-arrayexpress
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2020-07-02 | E-MTAB-8864 | biostudies-arrayexpress
Project description:Activated brown adipose tissue contributes to control of energy and glucose homeostasis in rodents and humans. Defining cell-autonomous processes underlying BAT differentiation and activation may thus reveal novel therapeutic targets for obesity and type 2 diabetes mellitus intervention. Here we show that ageing- and obesity-associated demises in BAT function coincide with down-regulation of mature microRNAs in BAT in the presence of reduced expression of the critical microRNA processing enzyme Dicer1. To mimic this partial down-regulation of microRNA processing in obesity and ageing, we inactivated one allele of Dicer1 selectively in BAT of mice. BAT- restricted heterozygosity of Dicer1 caused glucose intolerance in lean mice and aggravated diet-induced-obesity (DIO)-evoked deterioration of glucose homeostasis. Using combinatorial analyses of altered microRNA-expression in BAT during in vitro preadipocyte commitment and mouse models of progeria, longevity and DIO, we identified 23 microRNAs dysregulated among these conditions. Of these, we identified miR-328 as a novel regulator of BAT differentiation. miR-328 over-expression promotes BAT-differentiation and impairs muscle progenitor commitment, while reducing miR-328 expression blocks BAT specification. We validated the ß-Secretase Bace1 as a target of miR-328, which is consequently over-expressed in BAT of obese and premature ageing mice. Reducing Bace1 expression enhances brown adipocyte, while impairing myogenic differentiation in vitro. In vivo small-molecule Bace1 inhibition in obese mice delayed DIO-induced weight gain, ameliorated obesity-associated deterioration of glucose metabolism and improved insulin sensitivity. Collectively, these experiments reveal reduced Dicer1-miR-328-Bace1 axis in presence of generalized impairment of microRNA processing in ageing and obesity as a novel determinant of ageing- and obesity-associated decline in BAT function. This may define in vivo Bace1-inhibition as an innovative therapeutic approach to not only target age-related neurodegenerative diseases but at the same time improving age-related impairment of BAT-function and metabolism. C57BL/6 mice ( 4 weeks of age) were treated with a calory-rich, high-sugar high-fat diet (HFD) for a course of 4 weeks. Then groups were stratified and one group continued to receive HFD (BAT13-15) or HFD supplemented with an experimental small-molecule Bace 1 inhibitor (BAT17, 33, 35).
2015-06-17 | E-GEOD-69913 | biostudies-arrayexpress
Project description:Neuroplastic changes in the dorsal striatum participate in the transition from casual drug use to habitual and compulsive drug taking. These alterations might also play a critical role in the development of methamphetamine (METH) addiction. Nevertheless, the molecular substrates that underlie habitual METH consumption have yet to be elucidated. Therefore, in the present study, we examined the influence of METH self-administration on the expression of genes and proteins of interest, as potential substrates of METH-induced neuronal plasticity in the dorsal striatum. Rats self-administered METH (0.1 mg/kg/injection, i.v.) during 15 h sessions for 8 d and were euthanized after 2 h, 24 h, or 1 month of abstinence. Compared to yoked saline control, METH self-administration induced increases in the mRNA expression of the transcription factors, c-fos and fosb, the neurotrophic factor, Bdnf, and of the synaptic protein, synaptophysin (Syp) at 2 h after cessation of drug exposure. METH self-administration also caused changes in FosB, BDNF and TrkB protein levels, with increases at 2 and 24 h but decreases observed after 1 month of drug abstinence. Importantly, METH exposure caused increases in the levels of H3K4me3 and pCREB after 2 and 24 h of abstinence. Chromatin immunoprecipitation followed by qPCR was used to clarify the role of these proteins in the regulation of gene expression. We found that METH self-administration caused enrichment of pCREB, but not of H3K4me3, on the promoters of c-fos, fosb, Bdnf and Syp at 2 h after drug cessation. These data indicate that METH-induced activation of their transcription is mediated, in part, by pCREB-dependent epigenetic phenomena. Thus, METH self-administration might trigger epigenetic changes that caused alterations in the expression of genes and proteins serving as substrates for addiction-related synaptic plasticity. Animals were trained to self-administer METH for 8 d as described in the paper, dorsal striata were isolated 2 h, 24 h and 1 month after the final self-administration session. RNA extraction, RNA labeling and microarray hybridization were performed. In brief, total RNA was isolated from the samples using RNeasy Mini Kit (QIAGEN, Valencia, CA). RNA concentration and integrity was determined using Agilent BioAnalyzer (Agilent, Santa Clara, CA). Samples were stored at -80ºC. Microarray hybridization was done using RatRef-12 Expression BeadChips arrays (22 523 probes) (Illumina Inc., San Diego, CA). A 600 ng of total RNA from each sample was amplified using Illumina RNA Amplification kit (Ambion, Austin, TX). Single-stranded RNA (cRNA) was generated and labeled by incorporating biotin-16-UTP (Roche Diagnostics, Indianapolis, IN). 750 ng of each cRNA sample were hybridized to Illumina arrays at 55°C overnight according to the Gene Expression Protocol for BeadStation (Illumina Inc.). Hybridized cRNA was detected with cyanine3-streptavidin (GE Healthcare, Piscataway, NJ) and quantified using Illumina's BeadStation 500GX scanner.
2012-05-31 | E-GEOD-38223 | biostudies-arrayexpress
Project description:The tissue stroma plays a major role in tumors natural history. Important programs for tumor progression such as epithelial mesenchymal transition are not activated as cell-autonomous processes but under the conditions of cross-talk between tumor and stroma. Adipose tissue is a major component of the stroma and, because of their extended half-life, adipocytes are witnesses of tissue exposures. This study compares breast fat in women with breast tumors to those in healthy women to try to define a signature that could be translated into biomarkers for cancer and / or cancer risk. In the tumor-bearing breasts, we sampled adipose tissues adjacent to or distant from the tumor. Parameters studied include: adipocytes size and density; immune cells infiltration, vascularization, functional excretion and gene expression. Adipose tissues from tumor-bearing breasts whether adjacent to or distant from the tumor, did not differ from each other by any of these parameters. By contrast, when compared to adipose tissues from tumor-free breasts, tissues from tumor-bearing breasts displayed functional characteristics pointing to some sort of \\"activation\\". They have the capacity to excrete twice as much of interleukin 8 (p=0.001) and they differentially express a set of around 200 genes, at a threshold of p-value 0.001, of which many belong to inflammation mediated by chemokine and cytokine signaling and integrin signaling pathways. The presence of mast cells appears as a strong predictor of IL-8 secretion capacity (Log2 scale p = 0.002). Therefore, breast fat tissues from breast cancer patients have distinct functional and expression profiles. Although a dialogue effect with the tumor cannot be ruled out, it is also possible that this status is individually defined thus determining the constitutive permissiveness of the tissue for the development of cancer. The activation of pathways that was observed could potentially be translated into biomarkers or therapeutic targets. This transcriptomic analysis has been performed on two types of samples at short and long distances from the tumour in comparison with samples from normal tissues on Illumina beadarrays.
2020-10-05 | E-MTAB-8638 | biostudies-arrayexpress