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The peroxisome proliferator-activated receptor-gamma agonist pioglitazone modulates aberrant T cell responses in systemic lupus erythematosus

ABSTRACT: Previous studies indicate that peroxisome proliferator-activated receptor-gamma (PPAR-g) agonists suppress autoimmune responses and renal inflammation in murine lupus. However, the mechanisms implicated in this process remain unclear. We tested the effect of the PPAR-g agonist pioglitazone in human lupus and control PBMCs with regards to gene regulation and various functional assays. We used microarrays to analyze the effect of Pioglitazone on peripheral blood cells (PBMCs) from healthy and lupus patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE45923 | GEO | 2014/12/08

SECONDARY ACCESSION(S): PRJNA196646

REPOSITORIES: GEO

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The peroxisome proliferator-activated receptor-gamma agonist pioglitazone modulates aberrant T cell responses in systemic lupus erythematosus

Project description:Previous studies indicate that peroxisome proliferator-activated receptor-gamma (PPAR-g) agonists suppress autoimmune responses and renal inflammation in murine lupus. However, the mechanisms implicated in this process remain unclear. We tested the effect of the PPAR-g agonist pioglitazone in human lupus and control PBMCs with regards to gene regulation and various functional assays. We used microarrays to analyze the effect of Pioglitazone on peripheral blood cells (PBMCs) from healthy and lupus patients. Human PBMCs were isolated; RNA from healthy and lupus PBMCs was extracted and processed for hybridization on Affymetrix microarrays. Samples are paired as follows: 1-2, 3-4, 5-6, 7-8, 9-10, 11-12, 13-14, 15-16, 19-20.

2014-12-08 | E-GEOD-45923 | biostudies-arrayexpress

The peroxisome-proliferator activated receptor-? agonist pioglitazone modulates aberrant T cell responses in systemic lupus erythematosus.

Project description: Not available

| S-EPMC4184099 | biostudies-literature

Pioglitazone, a Peroxisome Proliferator-Activated Receptor ? Agonist, Suppresses Rat Prostate Carcinogenesis.

Project description: Not available

| S-EPMC5187871 | biostudies-other

Different skeletal effects of the peroxisome proliferator activated receptor (PPAR)alpha agonist fenofibrate and the PPARgamma agonist pioglitazone.

Project description: Not available

| S-EPMC2678137 | biostudies-literature

The peroxisome proliferator-activated receptor-gamma agonist pioglitazone represses inflammation in a peroxisome proliferator-activated receptor-alpha-dependent manner in vitro and in vivo in mice.

Project description: Not available

| S-EPMC2633943 | biostudies-literature

Pioglitazone ameliorates gentamicin ototoxicity by affecting the TLR and STAT pathways in the early postnatal organ of Corti

Project description:We evaluated the effects of pioglitazone in mouse organ of Corti (OC) explants to characterize its influence on signaling pathways involved in auditory hair cell damage. Organ of Corti explants were cultured with pioglitazone, gentamicin, or a combination of both agents. Pioglitazone treatment resulted in a significant repression of interferon (IFN)-alpha and -gamma pathways and downstream cytokines, as assessed by RNA sequencing and quantitative PCR gene expression assays. More detailed investigation at the single gene and protein level showed that pioglitazone mediated its anti-inflammatory effects through alterations of the Toll-like receptor (TLR) and STAT pathways. Together, these results indicate that pioglitazone significantly represses IFN and TLR in the cochlea, dampening the activity of gentamicin-induced pathways. These data support our previous results demonstrating significant protection of auditory hair cells in organ of Corti explants exposed to pioglitazone and other PPAR-targeted agents.

2020-09-24 | GSE158431 | GEO

Defining the cellular proteolytic landscape in systemic lupus erythematosus

Project description:Mass spectrometry analysis of cellular targets of protein degradation in PBMCs of healthy individuals and systemic lupus

2018-10-11 | PXD009112 | Pride

Bladder-cancer-associated mutations in RXRA activate peroxisome proliferator-activated receptors to drive urothelial proliferation

Project description:RXRA regulates transcription as part of a heterodimer with 14 other nuclear receptors, including the peroxisome proliferator-activated receptors (PPARs). Analysis from the TCGA raised the possibility that hyperactive PPAR signaling, either due to PPAR gamma gene amplification or RXRA hot-spot mutation (S427F/Y) drives 20-25% of bladder cancers. Here we characterize mutant RXRA, demonstrating it induces enhancer/promoter activity in the context of RXRA/PPAR heterodimers. Structure-function studies indicate the RXRA substitution allosterically regulates the PPAR AF2 domain via an aromatic interaction with the terminal tyrosine found in PPARs. In urothelium, we find PPAR agonism is sufficient to drive growth factor independent growth, but only after deletion of the tumor suppressors Kdm6a and Trp53. Similarly, mutant RXRA stimulates growth factor independent growth, in a manner reversible by PPAR inhibition. These studies reveal a pro-tumorigenic interaction between loss of tumor suppressors and PPAR activation and implicate PPARs as targetable drivers of bladder cancer.

2017-12-07 | GSE107735 | GEO

Bladder Cancer Associated Mutations in RXRA activate Peroxisome Proliferator-Activated Receptors to Drive Urothelial Proliferation

2017-12-07 | GSE107734 | GEO

Pioglitazone treatment of Lethal Yellow mice

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

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