Expression data of human coronary artery perivascular adipocytes and subcutaneous adipocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Rebekah Karns
PROVIDER: E-GEOD-45169 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Inflammatory crosstalk between perivascular adipose tissue and and blood vessel wall may contribute to atherosclerosis pathogenesis, and exhibits more pro-inflammatory than adipogenic phenotype than subcutaneous adipocytes. To identify a genomic basis for biologic differences, we performed genome-wide expression to identiy expression genes differentially regulated between perivascular and subcutaneous adipocytes.for biologic differences.
2013-03-15 | GSE45169 | GEO
Project description:Visceral adiposity is a risk factor for severe COVID-19 and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 undergoes productive infection in adipocytes, although the degree of infection and the cellular response depend on the anatomical origin of the adipocyte and the viral strain. Differentiated adipocytes from human visceral adipose tissue are more permissive to SARS-CoV-2 infection than their subcutaneous counterpart, and this associates with ACE2 expression. Infection of subcutaneous adipocytes leads to inhibition of lipolysis, while infection of visceral adipocytes results in higher expression of pro-inflammatory cytokines. Infected adipocytes begin to die 4 days after infection, regardless of the origin. The viral load and cellular response are attenuated when adipocytes are infected with the SARS-CoV-2 variant P.1. Hence, SARS-CoV-2 infects and replicates in adipocytes, where it compromises cell viability and alters lipid metabolism or elicits a pro-inflammatory response depending on the fat depot and the viral strain.
2024-02-29 | PXD030910 | Pride
Project description:Adipose tissue abundance relies partly on the factors that regulate adipogenesis, i.e. proliferation and differentiation of adipocytes. While the transcriptional program that initiates adipogenesis is well-known, the importance of microRNAs in adipogenesis is less well studied. We thus set out to investigate whether miRNAs would be actively modulated during adipogenesis and obesity. Several models exist to study adipogenesis in vitro, of which the cell line 3T3-L1 is probably the most well known, albeit not the most physiologically appropriate. We used a microarray strategy to provide a global profile of miRNAs in brown and white primary murine adipocytes (prior to and following differentiation) and evaluated the similarity of the responses to non-primary cell models, through literature data-mining. We found 65 miRNAs regulated during in vitro adipogenesis in primary adipocytes. When we compared our primary adipocyte profiles with those of cell lines reported in the literature, we found a high degree of difference in adipogenesis-regulated miRNAs. We evaluated the expression of 10 of our adipogenesis-regulated miRNAs using real-time qPCR and then selected 5 miRNAs that showed robust expression levels and profiled these by qPCR in subcutaneous adipose tissue of 20 humans with a range of body mass indices (BMI, range=21-48). Of the miRNAs tested, mir-21 was both highly expressed in human adipose tissue and positively correlated with BMI (R2=0.49, p<0.001). In conclusion, we provide the preliminary analysis of miRNAs important for primary cell in vitro adipogenesis and find that the inflammation-associated miRNA, mir-21, is up-regulated in subcutaneous adipose tissue in human obesity. A global transcriptomic survey of subcutaneous adipose tissue from human subjects characterised as having normal glucose tolerance, glucose intolerance or frank type 2 diabetes.
2011-05-31 | E-GEOD-27949 | biostudies-arrayexpress
Project description:Background/aims: Serum concentrations of the hepatokine fibroblast growth factor (FGF) 21 are elevated in obesity, type‐2 diabetes, and the metabolic syndrome. We asked whether FGF21 levels differ between subjects with metabolically healthy vs. unhealthy obesity (MHO vs. MUHO) opening the possibility that FGF21 is a cross‐talker between liver and adipose tissue in MUHO. Furthermore, we studied the effects of chronic FGF21 treatment on adipocyte differentiation, lipid storage, and adipokine secretion. Methods/study design: In 20 morbidly obese donors of abdominal subcutaneous fat biopsies discordant for their whole‐body insulin sensitivity (hereby classified as MHO or MUHO subjects), serum FGF21 was quantified. The impact of chronic FGF21 treatment on differentiation, lipid accumulation, and adipokine release was assessed in isolated preadipocytes differentiated in vitro. Results: Serum FGF21 concentrations were more than two‐fold higher in MUHO as compared to 37 MHO subjects (457 ±378 vs. 211 ±123 pg/mL; p<0.05). FGF21 treatment of human preadipocytes for the entire differentiation period was modestly lipogenic (+15%; p<0.05), reduced the expression of key adipogenic transcription factors (PPARG and CEBPA, ‐15% and ‐40%, respectively; p<0.01 both), reduced adiponectin expression (‐20%; p<0.05), markedly reduced adiponectin release (‐60%; p<0.01), and substantially increased leptin (+60%; p<0.01) and interleukin‐6 (+50%; p<0.001) release. Interpretation/conclusions: The hepatokine FGF21 exerts weak lipogenic and anti‐adipogenic actions and marked adiponectin‐suppressive and leptin and interleukin‐6 release‐promoting effects in human differentiating preadipocytes. Together with the higher serum concentrations in MUHO subjects, our findings reveal FGF21 as a circulating factor promoting the development of metabolically unhealthy adipocytes. We analysed in vitro differentiated preadipocytes from 20 human donors treated with FGF21 or control cultures.
2015-05-19 | E-GEOD-67279 | biostudies-arrayexpress
Project description:Bisphenol A (BPA) is a xenobiotic endocrine disrupting chemical. In vitro and in vivo studies indicated that BPA alters endocrine-metabolic pathways in adipose tissue increasing the risk of developing metabolic disorders. BPA effects on human adipocytes, specifically in children, are poorly investigated. To investigate in childhood the effect of exposure to BPA on metabolic disorders we analyzed in vitro the effects of environmentally relevant doses of BPA on gene expression of mature human adipocytes from pre-pubertal lean patients and on related physiological outcomes. Adipocytes from children were treated in vitro with BPA and gene expression was evaluated by qRT-PCR. Genome wide analyses were performed using GeneChip Human Gene 1.0 ST array. Lipid content in adipocytes was estimated by ORO staining and Triglyceride Quantification Kit. Secreted IL-1beta, in adipocytes culture medium, and insulin, in PANC-1 culture medium, were performed using ELISA assays. BPA was found to promote up-regulation of ER? and ERR?, and down-regulation of GPR30 expression modulating estrogen signaling and following a non-linear dose-response. Microarray data analysis demonstrated that BPA increases the gene expression of pro-inflammatory cytokines and lipid metabolism-related FABP4 and CD36 in adipocytes. PCSK1 resulted the most interesting gene being down-regulated by BPA thus impairing insulin production in pancreas. BPA promotes inflammation and lipid metabolism dysregulation in adipocytes from lean children. Moreover, PCSK1 can be a key gene in BPA action modulating insulin production. Exposure to BPA in childhood may be an important risk factor in developing obesity and metabolic disorders. Three prototypic situations were analyzed (5 replication each): untreated cells (C), 10 nM BPA treated cells (BPA), 1 nM 17-beta Estradiol treated cells (ES).
2015-07-09 | E-GEOD-58516 | biostudies-arrayexpress
Project description:Obesity is an epidemic health problem worldwide that impacts the risk and prognosis of many diseases. However, not all obese patients have the same risk of developing these disorders. Individuals with peripheral obesity, i.e., fat distributed subcutaneously, are at little or no risk of the common medical complications of obesity, whereas individuals with central obesity, i.e., fat accumulated in visceral depots, are prone to these complications. In the present study, using microaarays gene expression, we have explored the hypothesis that patterns of fat distribution and, perhaps, to some degree, obesity itself may have a developmental genetic origin. Experiment Overall Design: Isolated adipocytes and stromo-vascular fraction (SVF) of subcutaneous and intraabdominal adipose tissue of mice were used for RNA extraction and hybridization on Affymetrix microarrays. Three samples from each categories were used for the analyse.
2007-10-31 | E-GEOD-8505 | biostudies-arrayexpress
Project description:Adipose tissue abundance relies partly on the factors that regulate adipogenesis, i.e. proliferation and differentiation of adipocytes. While the transcriptional program that initiates adipogenesis is well-known, the importance of microRNAs in adipogenesis is less well studied. We thus set out to investigate whether miRNAs would be actively modulated during adipogenesis and obesity. Several models exist to study adipogenesis in vitro, of which the cell line 3T3-L1 is probably the most well known, albeit not the most physiologically appropriate. We used a microarray strategy to provide a global profile of miRNAs in brown and white primary murine adipocytes (prior to and following differentiation) and evaluated the similarity of the responses to non-primary cell models, through literature data-mining. We found 65 miRNAs regulated during in vitro adipogenesis in primary adipocytes. When we compared our primary adipocyte profiles with those of cell lines reported in the literature, we found a high degree of difference in adipogenesis-regulated miRNAs. We evaluated the expression of 10 of our adipogenesis-regulated miRNAs using real-time qPCR and then selected 5 miRNAs that showed robust expression levels and profiled these by qPCR in subcutaneous adipose tissue of 20 humans with a range of body mass indices (BMI, range=21-48). Of the miRNAs tested, mir-21 was both highly expressed in human adipose tissue and positively correlated with BMI (R2=0.49, p<0.001). In conclusion, we provide the preliminary analysis of miRNAs important for primary cell in vitro adipogenesis and find that the inflammation-associated miRNA, mir-21, is up-regulated in subcutaneous adipose tissue in human obesity. 3 samples of pre adipocytes isolated from brown adipose tissue examined pre and post differentiation to brown adipocytes. 3 samples of pre-adipocytes isolated from white adipose tissue and examined pre and post differentiation to adipocytes.
2011-05-31 | E-GEOD-27912 | biostudies-arrayexpress
Project description:Previous publications demonstrated that there were anatomical, physiological, cellular, clinical and prognostic differences among adipose tissue present in subcutaneous areas, abdominal cavity and outside adventitial layer of artery. Thus, we wondered whether ASCs from subcutaneous adipose tissue, abdominal adipose tissue and perivascular adipose tissue were also different in gene expression. Here we performed bulk RNA-Seq assay for subcutaneous, abdominal and perivascular adipose derived stem cells.
2021-04-13 | GSE171946 | GEO
Project description:Adipose tissue is a primary regulator of energy balance and metabolism. The distribution of adipose tissue depots is of clinical interest because the accumulation of upper-body subcutaneous (ASAT) and visceral adipose tissue (VAT) is associated with cardiometabolic diseases, whereas lower-body gluteal-femoral adipose tissue (GFAT) appears to be protective. There is heterogeneity in the morphological and metabolic traits of adipocytes obtained from different regions of the body, but detailed knowledge of the constituent proteins in each depot is lacking. Here, we determined the human adipocyte proteome from ASAT, VAT and GFAT using high-resolution SWATH mass spectrometry proteomics.
2021-04-19 | PXD018314 | Pride
Project description:Adipose tissue is one of the main regulative sites for energy metabolism. Excess lipid storage and expansion of white adipose tissue (WAT) is the primary contributor to obesity, a strong predisposing factor for development of insulin resistance. Sentrin-specific protease (SENP) 2 has been shown to play a role in metabolism in murine fat and skeletal muscle cells, and we have previously demonstrated its role in energy metabolism of human skeletal muscle cells. In the present work, we have investigated the impact of SENP2 on fatty acid and glucose metabolism in primary human fat cells by using cultured primary human adipocytes to knock down the SENP2 gene. Glucose uptake and oxidation, as well as accumulation and distribution of oleic acid into complex lipids were decreased while oleic acid oxidation was increased in SENP2-knockdown cells compared to control cells. Furthermore, de novo lipogenesis was reduced by SENP2-knockdown in the adipocytes and expression of several metabolically important regulators and markers of browning of WAT were upregulated both on gene and protein level. In conclusion, SENP2 is an important regulator of energy metabolism in primary human adipocytes, and the results indicates a potential role in browning of the cells as well.
2023-02-10 | PXD033508 | Pride