Expression data of Pioglitazone-, Rosiglitazone-, GW1929- and vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+Pparg1
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE37534 | GEO | 2012/05/04
SECONDARY ACCESSION(S): PRJNA161107
REPOSITORIES: GEO
Similar Datasets
Project description:Pioglitazone treatment of CD4+FoxP3- T cells transduced with Pparg and Foxp3 up-regulated a set of genes whose products have been implicated in lipid metabolism pathways. To verify the specificity of this treatment, we performed microarray analysis on Foxp3+Pparg1-transduced CD4+FoxP3- T cells after treatment with other PPARg agonists such as Rosiglitazone (TZD) and GW1929 (non-TZD). All gene expression profiles were obtained from highly purified (double-sorted) T cell populations sorted by flow cytometry. To reduce variability, cells from multiple mice were pooled. Triplicates were generated for all groups. Raw data were preprocessed with the RMA algorithm in GenePattern and averaged expression values were used for analysis.
2012-05-03 | E-GEOD-37534 | biostudies-arrayexpress
Project description:We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis.
2012-05-04 | GSE37533 | GEO
Project description:We identified Pparg as a major orchestrator of the phenotype of adipose-tissue resident regulatory T cells (VAT Tregs). To explore the contribution of Pparg1 and 2 in the generation of the VAT Tregs-specific gene signatures, CD4+FoxP3- T cells were transduced with Foxp3+/- Pparg1 (or Pparg2), treated with Pioglitazone or vehicle, and double sorted for microarray analysis. All gene expression profiles were obtained from highly purified (double-sorted) T cell populations sorted by flow cytometry. To reduce variability, cells from multiple mice were pooled. Triplicates were generated for all groups. Raw data were preprocessed with the RMA algorithm in GenePattern and averaged expression values were used for analysis.
2012-05-03 | E-GEOD-37533 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE37532: Gene expression profile of regulatory T cells (Tregs) isolated from visceral adipose tissue and lymph nodes of mice sufficient and deficient of Pparg expression in Tregs GSE37533: Expression data of Pioglitazone- or vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+/- Pparg1 (or Pparg2) GSE37534: Expression data of Pioglitazone-, Rosiglitazone-, GW1929- and vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+Pparg1 Refer to individual Series
2012-05-03 | E-GEOD-37535 | biostudies-arrayexpress
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.
2022-03-25 | GSE186277 | GEO
Project description:Goal of the experiment: To examine differential gene expression in the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice treated with vehicle or pioglitazone. Brief description of the experiment: The objective of this study was to use whole mouse genome DNA microarrays (Codelink) to examine gene expression the ovaries of heterozygous Lethal Yellow (C57BL/6J Ay/a) mice. Women with polycystic ovary syndrome (PCOS) treated with thiazolidinediones (TZD), such as pioglitazone, show reduced androgen levels and improved ovulatory function. Recent evidence suggests that TZD, acting via peroxisome proliferator-activated receptor gamma (PPAR gamma), alter the expression of ovarian genes involved in insulin/IGF signaling that may account for some of the observed effects. Since TZD can alter the expression of a large variety of genes, there may be other mechanisms involved in the improvement of ovarian function with TZD treatment. Lethal yellow (LY) mice exhibit progressive obesity, reproductive dysfunction, and altered metabolic regulation (e.g. insulin and leptin resistance) similar to women with PCOS. This study was designed to test the hypothesis that prolonged treatment of aging LY mice with pioglitazone would alter the expression of ovarian genes involved in reproduction. Beginning at 120-days and continuing until 180-days of age, female LY mice received daily oral doses of either 0.1 mg pioglitazone (n = 4) or an equal volume of vehicle (0.1 ml 100% DMSO; n = 4). At the end of the treatment regimen, ovaries were removed and RNA extracted. Total RNA extracts were run individually on Codelink Mouse Whole Genome Bioarrays (GE). Relative gene expression was compared between treatments by t-test using GeneSpring software. Keywords: mouse, drug treatment Experimental factors: drug treatment Keywords: drug treatment
2008-07-08 | GSE8806 | GEO
Project description:Expression data of Pioglitazone- or vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+/- Pparg1 (or Pparg2)
| PRJNA161105 | ENA
Project description:Expression data of Pioglitazone-, Rosiglitazone-, GW1929- and vehicle-treated CD4+FoxP3- T cells transduced with Foxp3+Pparg1
| PRJNA161107 | ENA
Project description:Insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes. Studies have shown that thiazolidinediones (TZD) improve metabolic disturbances in PCOS patients. We hypothesized that the effect of TZD in PCOS is in part mediated by changes in the transcriptional profile of muscle favoring insulin sensitivity. Using Affymetrix microarrays, we examined the effect of pioglitazone (30 mg/day for 16 weeks) on gene expression in skeletal muscle of 10 obese women with PCOS metabolically characterized by a euglycemic-hyperinsulinemic clamp. Moreover, we explored gene expression changes between these PCOS patients before treatment and 13 healthy control women. Treatment with pioglitazone improved insulin-stimulated total, oxidative and non-oxidative glucose metabolism, and reduced fasting serum insulin (all p < 0.05). Global pathway analysis using Gene Map Annotator and Pathway Profiler (GenMAPP 2.1) and Gene Set Enrichment Analysis (GSEA 2.0.1) revealed a significant upregulation of genes involved in mitochondrial oxidative phosphorylation (OXPHOS), ribosomal proteins, mRNA processing reactome, translation factors, and proteasome complexes in PCOS patients after pioglitazone therapy. Quantitative real-time PCR suggested that upregulation of OXPHOS genes was mediated by an increase in PGC-1α expression (p < 0.05). Expression of genes involved in ribosomal proteins and OXPHOS was down-regulated in PCOS patients before treatment compared to matched healthy women using GenMAPP 2.1 and GSEA 2.1. These data indicate that pioglitazone therapy restores insulin sensitivity in part by a coordinated upregulation of genes involved in mitochondrial oxidative metabolism and protein biosynthesis in skeletal muscle of PCOS. These transcriptional effects of pioglitazone therapy may contribute to prevent the onset of type 2 diabetes in these women. Keywords: PCOS, microarray, global pathway analysis, insulin resistance, pioglitazone, protein metabolism, mitochondrial oxidative metabolism
2008-11-10 | GSE8157 | GEO
Project description:Insulin resistance is a common metabolic abnormality in women with PCOS and leads to an elevated risk of type 2 diabetes. Studies have shown that thiazolidinediones (TZD) improve metabolic disturbances in PCOS patients. We hypothesized that the effect of TZD in PCOS is in part mediated by changes in the transcriptional profile of muscle favoring insulin sensitivity. Using Affymetrix microarrays, we examined the effect of pioglitazone (30 mg/day for 16 weeks) on gene expression in skeletal muscle of 10 obese women with PCOS metabolically characterized by a euglycemic-hyperinsulinemic clamp. Moreover, we explored gene expression changes between these PCOS patients before treatment and 13 healthy control women. Treatment with pioglitazone improved insulin-stimulated total, oxidative and non-oxidative glucose metabolism, and reduced fasting serum insulin (all p < 0.05). Global pathway analysis using Gene Map Annotator and Pathway Profiler (GenMAPP 2.1) and Gene Set Enrichment Analysis (GSEA 2.0.1) revealed a significant upregulation of genes involved in mitochondrial oxidative phosphorylation (OXPHOS), ribosomal proteins, mRNA processing reactome, translation factors, and proteasome complexes in PCOS patients after pioglitazone therapy. Quantitative real-time PCR suggested that upregulation of OXPHOS genes was mediated by an increase in PGC-1M-NM-1 expression (p < 0.05). Expression of genes involved in ribosomal proteins and OXPHOS was down-regulated in PCOS patients before treatment compared to matched healthy women using GenMAPP 2.1 and GSEA 2.1. These data indicate that pioglitazone therapy restores insulin sensitivity in part by a coordinated upregulation of genes involved in mitochondrial oxidative metabolism and protein biosynthesis in skeletal muscle of PCOS. These transcriptional effects of pioglitazone therapy may contribute to prevent the onset of type 2 diabetes in these women. Experiment Overall Design: Ten obese women of reproductive age with PCOS participated in the study to test the effect of pioglitazone therapy (data set 1). To test if pioglitazone ameliorate existing defects in PCOS patients, the expression profile of the 10 PCOS patients before treatment were compared to the same cohort of 13 control subjects (data set 2).
2008-11-14 | E-GEOD-8157 | biostudies-arrayexpress