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Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (miRNA)

ABSTRACT: The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE68604 | GEO | 2018/05/05

REPOSITORIES: GEO

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Trancriptional profiling of rat bladder after daily administration of Pioglitazone and Rosiglitazone in vivo (mRNA)

Project description:The purpose of the study was to investigate the nongenotoxic carcinogenic effect of Pioglitazone. Pioglitazone is a PPARgamma agonist and is known to cause bladder tumours in male rats and an increase in the incidence of bladder cancer in humans has been observed in patients treated with Pioglitazone. Pioglitazone is not considered genotoxic or carcinogenic in mice and tumours are only observed in male rats suggesting a nongenotoxic mechanism of tumorigenesis. A suggested hypothesis is urinary calculi formation and subsequent irritation, hyperplasia and metaplasia. Rosiglitazone was used as reference compound as this PPARgamma agonist does not cause changes in the bladder but cause lipoma/liposarcoma in rats.

2018-05-05 | GSE68592 | GEO

Endogenous vitamin E metabolites mediate allosteric PPARγ activation with unprecedented co-regulatory interactions

Project description:Effects of the PPARgamma ligands pioglitazone and garcinoic acid on gene expression in HepG2 cells

2021-04-16 | E-MTAB-10328 | biostudies-arrayexpress

Comparison of the transcriptomic profile of intestinal epithelial cells (Caco-2 cells) treated with different PPARgamma agonists

Project description:Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor highly expressed by colonic epithelial cells. It plays a key role in gut homeostasis and metabolism regulation. We previously showed that PPARgamma has a role in the action of aminosalycilates (5-ASA), one of the oldest anti-inflammatory agents used in the treatment of inflammatory bowel disease. These data have prompted us to develop novel analogues of 5-ASA with greater PPARgamma-activating properties (GED). The various PPARgamma ligands appear to have some markedly different effects, some of which can induce adverse effects. The transcriptomic profiles induced by various families of PPARgamma ligands are very poorly known and especially in intestinal epithelial cells. Hence, the objectives of the present project is to compare the gene expression profile induced by GED, 5-ASA, and pioglitazone in Caco-2 cells, in order to better understand these compounds’ modes of action, to discover potential new PPARgamma target genes in intestinal epithelial cells and to explain the efficacy difference between GED and 5-ASA.

2015-10-12 | GSE68852 | GEO

The expression profile of miRNA in the bladder tissue of partial bladder outlet obstruction rats before and after treatment of human urine-derived stem cells

Project description:Obstruction in any part between the outlet of the bladder and the external urethra is called partial Bladder outlet obstruction (pBOO), which is a common disease in urology, which may cause bladder dysfunction. We have comfirmed that human urine-derived stem cells (hUSCs) could improve the bladder function of pBOO rats in our previous study. We thus explored the role of miRNAs in pBOO rats before and after treatment of hUSCs, and revealed that they could serve as effective prevention and treatment therapeutic targets. Rat bladder tissues were used for miRNA sequencing. We identified 8 differentially expressed miRNAs in the pBOO rats before and after treatment of hUSCs.

2021-04-02 | GSE171293 | GEO

The expression profile of circRNA, lncRNA and mRNA in the bladder tissue of partial bladder outlet obstruction rats before and after treatment of human urine-derived stem cells

2021-04-02 | GSE171366 | GEO

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (miRNA)

Project description:In this study we performed microarray-based molecular profiling of liver samples from Wistar rats exposed to genotoxic carcinogens (GC), nongenotoxic carcinogens (NGC) or non-hepatocarcinogens (NC) for up to 14 days. In contrast to previous toxicogenomics studies aimed at the inference of molecular signatures for assessing the potential and mode of compound carcinogenicity, we considered multi-level omics data. Besides evaluating the predictive power of signatures observed on individual biological levels, such as mRNA, miRNA and protein expression, we also introduced novel feature representations which capture putative molecular interactions or pathway alterations by integrating expression profiles across platforms interrogating different biological levels. Male Wistar rats were treated by oral gavage with the eight nongenotoxic hepatocarcinogens Phenobarbital sodium (PB), Piperonylbutoxide (PBO), Dehydroepiandrosterone (DHEA), Acetamide (AA), Methapyrilene HCl (MPy), Methylcarbamate (Mcarb), Diethylstilbestrol (DES) and Ethionine (ETH), the two genotoxic carcinogens C.I Direct Black (CIDB) and dimethylnitrosamine (DMN), the two non-hepatocarcinogens Cefuroxime (CFX) and Nifedipine (Nif), and the three compounds with undefined carcinogenic class Cyproterone acetate (CPA), Thioacetamid (TAA) and Wy-14643 (Wy). Depending on the administered compound, livers were taken after 3, 7, or 14 days for histopathological evaluation. From the five animals per treatment group three animals were selected based on the histopathological findings and subjected to molecular profiling using Affymetrix RG-230A arrays (mRNA expression), Agilent G4473A arrays (miRNA expression) and Zeptosens ZeptoMARK reverse arrays (protein expression).

2014-08-18 | E-GEOD-53083 | biostudies-arrayexpress

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (mRNA)

2014-08-18 | E-GEOD-53082 | biostudies-arrayexpress

Cross-platform toxicogenomics for the prediction of nongenotoxic hepatocarcinogenesis in rat (protein)

2014-08-18 | E-GEOD-53084 | biostudies-arrayexpress

Effects of PPARgamma-inactive Delta-2-TGZ on breast cancer cells MCF-7

Project description:TGZ is an agonist of the nuclear receptor PPARgamma. This synthetic compound displays anticancer effects on breast cancer cells but some of them are PPARgamma independent. Delta-2-TGZ (delta-2-troglotazone) is a PPARgamma inactive TGZ derivative possessing a double bond adjoining the thiazolidinedione ring. This compound still displays anticancer efefcts. It is an interesting tool to study the PPARgamma-independent mechanisms. We used microarrays to examine the global programme of gene expression in response to Delta-2-TGZ treatment in MCF7 cell line.

2017-07-07 | GSE99941 | GEO

Comparative Transcriptional Network Modeling of Three PPAR-α/γ Co-agonists Reveals Distinct Metabolic Gene Signatures in Primary Human Hepatocytes

Project description:Aims: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor-α/γ (PPAR-α/γ) agonist, aleglitazar, with tesaglitazar (a dual PPAR-α/γ agonist) or combination of pioglitazone (PPAR-γ agonist)/fenofibric acid (PPAR-α agonist) in human hepatocytes. Methods and Results: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC50-aligned low, medium, and high concentrations of the three treatments. A systems-biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and pioglitazone/fenofibric acid, each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-α signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and pioglitazone/fenofibric acid, due to greater number of gene expression changes in pathways related to HDL and LDL metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, pioglitazone/fenofibric acid was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect. All treatments were inferred to decrease proliferative signaling. Conclusions: Aleglitazar induces transcriptional signatures related to lipid parameters and stress responses that are unique from other dual PPAR-α/γ treatments. This may underlie observed favorable changes in lipid profiles in animal and clinical studies with aleglitazar and suggests a differentiated gene profile compared with other dual PPAR-α/γ agonist treatments.

2011-10-22 | GSE33152 | GEO

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