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The effect of fenofibrate on endothelial cells

ABSTRACT: Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha, but there are reports that fenofibrate affects endothelial cells in PPARa-independent manner. In order to identify PPARa-dependently and PPARa-independently regulated transcripts we generated microarray data from human endothelial cells treated with fenofibrate with and without siRNA-mediated knock-down of PPARa.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15483 | GEO | 2009/08/24

SECONDARY ACCESSION(S): PRJNA122973

REPOSITORIES: GEO

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The effect of PPARa siRNA on endothelial cells treated with fenofibrate

2009-08-24 | GSE15482 | GEO

The effect of PPARa siRNA on endothelial cells treated with fenofibrate

Project description:Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha, but there are reports that fenofibrate affects endothelial cells in PPARa-independent manner. In order to identify PPARa-dependently and PPARa-independently regulated transcripts we generated microarray data from human endothelial cells treated with fenofibrate with and without siRNA-mediated knock-down of PPARa. In this study, we generated microarray data from human umbilical vein endothelial cells (HUVECs) treated with fenofibrate with pretreatment PPARa or control siRNA. There are four time points (4, 8, 12 and 18hours) (n=1 at each time point).

2009-08-24 | E-GEOD-15482 | biostudies-arrayexpress

The effect of fenofibrate on endothelial cells

Project description:Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha, but there are reports that fenofibrate affects endothelial cells in PPARa-independent manner. In order to identify PPARa-dependently and PPARa-independently regulated transcripts we generated microarray data from human endothelial cells treated with fenofibrate with and without siRNA-mediated knock-down of PPARa. In this study, we generated microarray data from human umbilical vein endothelial cells (HUVECs) treated with fenofibrate. Time 0 indicates the start point of observation immediately prior to exposure to the 25umol fenofibrate. There are five time points (2, 4, 6, 8, and 18hours) (n=3 at each time point). The control is untreatment HUVEC (n=4).

2010-05-06 | E-GEOD-15483 | biostudies-arrayexpress

Human umbilical vein endothelial cells (HUVECs) treated with fenofibrate

Project description:This SuperSeries is composed of the following subset Series: GSE15482: The effect of PPARa siRNA on endothelial cells treated with fenofibrate GSE15483: The effect of fenofibrate on endothelial cells Refer to individual Series

2009-08-24 | E-GEOD-15494 | biostudies-arrayexpress

Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice treated or not with Fenofibrate

Project description:Fenofibrate is a specific agonist of the nuclear receptor PPARa. To identify the gene expression under the strict dependence of hepatic PPARa activity, we generated a new mouse strain of PPARa-specific deletion in hepatocyte (albumin-Cre+/- Pparaflox/flox or LKO) and we compared them to total Ppara KO (KO), wild-type (WT) and liver WT (albumin-Cre-/- Pparaflox/flox or LWT) mice. We used microarrays to detail the global programme of gene expression in liver of Ppara LKO, LWT, Ppara KO and WT male mice. There are 36 liver samples, each from an individual mouse. The samples are from Ppara liver KO (LKO), Ppara KO (KO), wild-type (WT) and liver WT (LWT) male mice of 14 week-old from the same genetic background (C57Bl/6J) treated with Fenofibrate (100 mg/kg/day) or vehicle (aqueous solution of gum Arabic 3%) by daily gavage for 10 days. n= 4 mice for LKO, LWT and WT genotypes treated with vehicle; n=3 for KO mice treated with vehicle; n=5 mice for LWT, LKO and KO genotypes treated with fenofibrate; n=4 WT mice treated with fenofibrate. All mice were sacrified at ZT14.

2016-02-20 | E-GEOD-73298 | biostudies-arrayexpress

Suppression of PPAR α Protects Against Hypertrophy Associated Apoptosis of the Cardiomyocytes in Mice Heart

Project description:Cardiac hypertrophy is characterized by increase in the size of the cardiomyocytes which is initially triggered as an adaptive response due to various kinds of stimuli but ultimately becomes maladaptive with chronic exposure. Peroxisome proliferator activated receptor alpha (PPAR α), which is critical for mitochondrial biogenesis and fatty acid oxidation, is known to be down regulated in hypertrophied cardiomyocytes. The aim of the study was to unveil the role of PPAR α in the mechanism that drives myocardium towards maladaptation in chronic hypertrophy. Wild-type C57BL/6 and PPAR α-/- mice were subjected to isoproterenol treatment for 2 weeks (n=8). Proteomic analysis using Orbitrap mass spectrometer revealed an unexpected down regulation of apoptotic markers, Annexin V and p53. PPAR α regulated and non-regulated genes were validated using RT-PCR. Specificity for α isoform was confirmed using PPAR α agonist, fenofibrate and pan-agonist bezafibrate. Fenofibrate failed to restore PPAR α target genes, whereas bezafibrate managed to ameliorate the effects of isoproterenol for a subset of genes even in the absence of PPAR α. Autophagy markers like p62, Beclin1 and LC3 A/B were up regulated in PPAR α-/-mice therefore indicating an upsurge in autophagy. The results demonstrate hindrance to intrinsic apoptotic pathway and activation of autophagy in the absence of PPAR α in hypertrophic cardiomyocytes. Therefore, PPAR α signalling might act as a molecular switch between apoptosis and autophagy thereby playing a critical role in adaptive process in stress induced cardiomyocytes.

2022-04-04 | PXD025470 | Pride

Global hepatic gene expression data from PPARa liver KO, PPARa liver WT, PPARaKO and WT male mice treated or not with Fenofibrate

2016-02-20 | GSE73298 | GEO

Assessment of the Mode of Action Underlying the Effects of GenX in Mouse Liver and Implications for Assessing Human Health Risks

Project description:To investigate the potential role of peroxisome proliferator activated receptor–alpha (PPARa) activation in mice, RNA sequencing was conducted on paraffin-embedded liver sections from a 90-day toxicity study of GenX conducted in mice. the TempO-Seq platform was utilized for RNA sequencing data collection. Differentially expressed genes were identified for each treatment group, and gene set enrichment analysis was conducted using gene sets that represent biological processes and known canonical pathways. Significant enrichment of peroxisome signaling was evident in males and females exposed to 0.5 and 5 mg/kg GenX, with no enrichment at 0.1 mg/kg. PPAR signaling and fatty acid metabolism were among the most significantly enriched gene sets, and two gene sets specific to the PPARa subtype were also significantly enriched.

2020-03-01 | GSE135943 | GEO

Transcriptome analysis of the injected Ppara-KO mice overexpressing TFEB specifically in liver

Project description:Expression data from Ppara (peroxisome proliferator activated receptor alpha) KO mice injected with TFEB specifically in liver. In order to identify the effects of TFEB overexpression together with Ppara absence on the liver transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the injected mice

2013-04-20 | GSE41140 | GEO

ChIP-chip of BMP2 or control treated human pulmonary artery endothelial cells with anti-beta-catenin or anti-ppar-gamma antibodies on promoter regions

Project description:Reduced bone morphogenetic protein receptor (BMPR)2 expression in patients with pulmonary arterial (PA) hypertension (PAH), can impair PA endothelial cell (EC) function. We now characterize, in human PAECs, a novel BMPR2-mediated transcriptionally active complex between peroxisome proliferator-activated receptor (PPAR) gamma and beta-catenin (BC), and show that disruption of this complex impairs BMP mediated HPAEC survival. Using whole genome wide ChIP-Chip promoter analysis we delineate PPARG-BC dependent transcription of target genes that include apelin. Comparison of ppar-gamma and beta-catenin occupancy on promoter regions from human pulmonary artery endothelial cells after either treatment with BMP2 or control. A total of 8 samples were created using NimbleGen human HG18 promoter arrays.

2011-05-25 | E-GEOD-29489 | biostudies-arrayexpress

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