Expression data from the adipose tissue of mice fed a normal diet and a high fat diet.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE36492 | GEO | 2013/01/30
SECONDARY ACCESSION(S): PRJNA153533
REPOSITORIES: GEO
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Project description:To identify novel Peroxisome Proliferator-Activated Receptor gamma (PPARg) responsive secretory and/or transmembrane genes that is related to obesity, we integrated the expression data from the adipose tissue derived from obese mice with the other two data sets: expression profiling of adipocyte differentiation using ST2 cells and siRNA-mediated knockdown of Pparg during ST2 cell adipogenesis. We used microarrays to detect the up-regulated genes in adipose tissue derived from mice fed a high fat diet compared to a control. Total RNA from adipose tissue was obtained and from mice fed a high fat diet HFD32 (MOUSE_HFD) from 6 week-old to 18 week-old, or a normal diet CE-2 (MOUSE_ND) as a control. Pooled RNAs of each three animals were analyzed by the Affymetrix GeneChip microarray system.
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Project description:Peroxisome proliferator-activated receptor g (PPARg) is a nuclear receptor that is a vital regulator of adipogenesis, insulin sensitivity, and lipid metabolism. Activation of PPARg by antidiabetic thiazolidinediones (TZD) reverses insulin resistance but also leads to weight gain that limits the use of these drugs. There are two main PPARg isoforms, but the specific functions of each are not established. Here we generated mouse lines in which endogenous PPARg1 and PPARg2 were epitope-tagged to interrogate isoform-specific genomic binding, and mice deficient in either PPARg1 or PPARg2 to assess isoform-specific gene regulation. Strikingly, although PPARg1 and PPARg2 contain identical DNA binding domains, we uncovered isoform-specific genomic binding sites in addition to shared sites. Moreover, PPARg1 and PPARg2 regulated different set of genes in adipose tissue depots, suggesting distinct roles in adipocyte biology. Indeed, mice with selective deficiency of PPARg1 maintained body temperature better than wild type or PPARg2-deficient mice. Most remarkably, although TZD treatment improved glucose toleranceinsulin resistance in mice lacking either PPARg1 or PPARg2, the PPARg1-deficient mice were protected from TZD-induced body weight gain compared to PPARg2-deficient mice. Thus, PPARg isoforms have specific and separable metabolic functions that may be targeted to improve therapy for insulin resistance and diabetes.
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Project description:PPARg and C/EBPa cooperate to control preadipocyte differentiation (adipogenesis). However, the factors that regulate PPARg and C/EBPa expression during adipogenesis remain largely unclear. Here we show PTIP, a protein that associates with histone H3K4 methyltransferases, regulates PPARg and C/EBPa expression in mouse embryonic fibroblasts (MEFs) and during preadipocyte differentiation. PTIP deletion in MEFs leads to marked decreases of PPARg expression and PPARg-stimulated C/EBPα expression. Further, PTIP is essential for induction of PPARg and C/EBPa expression during preadipocyte differentiation. Deletion of PTIP impairs the enrichment of H3K4 trimethylation and RNA polymerase II on PPARg and C/EBPa promoters. Accordingly, PTIP-/- MEFs and preadipocytes all show striking defects in adipogenesis. Furthermore, rescue of the adipogenesis defect in PTIP-/- MEFs requires co-expression of PPARg and C/EBPa. Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight in mice. Thus, by regulating PPARg and C/EBPa expression, PTIP plays a critical role in adipogenesis.
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Project description:"Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile"
Monica Viladomiu1,2, Raquel Hontecillas1,2, Mireia Pedragosa1,2, Adria Carbo1,2, Stefan Hoops1,2, Pawel Michalak4,5, Katarzyna Michalak4, Richard L. Guerrant2,3, James K. Roche2,3, Cirle A. Warren2,3, Josep Bassaganya-Riera1,2*
1) Nutritional Immunology and Molecular Medicine Laboratory, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 2) Center for Modeling Immunity to Enteric Pathogens, Virginia Tech, Blacksburg, Virginia, United States of America, 3) Division of Infectious Disease and International Health, Center for Global Health, University of Virginia, Charlottesville, Virginia, United States of America, 4) Medical Informatics and Systems Division, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 5) Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, United States of America
E-mail: jbassaga@vt.edu
This model represents the interaction between Cdiff, miRNA146b, NCOA4, PPARg, IL10 and IL17. Simulation studies show an aberrant expression of miRNA146b with increasing concentrations of Cdiff over time, which results in decreased PPARg activation due to NCOA4 inhibition. As a final result, PPARg is unable to modulate effector and regulatory responses, since results show an upregulation of IL17 expression and downregulation of IL10 production.
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