Gene expression data of bezafibrate treated CD8+ T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE118659 | GEO | 2018/08/17
REPOSITORIES: GEO
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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
Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.
2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress
Project description:A functional interaction between peroxisome proliferator-activated receptor alpha (PPARalpha) and components of the circadian clock has been suggested; however, it remains to be clarified whether those transcriptional factors interact with each other to regulate the expression of their target genes. In this study, we used a ligand of PPARalpha, bezafibrate, to search the PPARalpha-regulated genes that express in a CLOCK-dependent circadian manner. Microarrays analyses using hepatic RNA isolated from bezafibrate treated-wild type, Clock mutant (Clk/Clk), and PPARalpha-null mice revealed that 136 genes are transcriptionally regulated by PPARalpha in a CLOCK-dependent manner. Clk/Clk mutant mice with Jcl:ICR background, wild-type mice with the same strain, and PPARalpha-null mice aged 6-12 weeks were housed under a 12 h light-12 h dark cycle [LD 12:12; lights on at Zeitgeber time (ZT) 0]. For chronic treatment of bezafibrate, mice were provided with either a normal diet or the same diet containing 0.5% w/w bezafibrate for 5 days. A white fluorescent lamp provided light (300 - 500 lux at cage level) during the day. To examine the transient effect of bezafibrate injection on hepatic gene expression, bezafibrate was dissolved in warm (~40 C) sterile corn oil (Sigma) at a concentration of 10 mg/ml and administered intraperitoneally (i.p.) in a single dose of 100 mg/kg body weight at ZT2. To examine the PPARalpha-regulated genes that express in a CLOCK-dependent manner in mice, we performed oligonucleotide microarray analysis at ZT14, when CLOCK/BMAL1 transcriptional activity is maximal, using RNA isolated from wild-type (n = 3), Clock mutant (n = 3), and PPARalpha-null mice (n = 3) treated with bezafibrate for 5 days, and control wild-type mice (n = 3). Livers were collected and frozen in liquid nitrogen. Total RNA (250 ng) was extracted using RNAiso.
2010-06-14 | E-GEOD-20513 | biostudies-arrayexpress
Project description:We performed gene expresion analysis of T cell treated with agonist of three isoform of PPAR. This analysis allowed us to explain why the activation of PPAR g is the best in boosting PD-1 blockade efficacy compared with other isoform activation. We demonstrated that activation of the PPAR-γ isoform specifically enhanced PD-1 blockade greater than activation of the other two PPAR isoforms (a and b) in mouse tumor model. Using the microarray assay we found genes that were most differentially regulated by PPAR agonist treatment were with a well-documented role in T cell biology, such as Ddx3y, Ifng, Il17c, Ccr3, Acrv1, Btk and metabolic process such as Pygl, P2rx1, Tph2, Kynu, and Ugt2b37. Therefore, microarray data has been useful to establish that activation of PPAR-g in T cell uniquely modulate genes, which include metabolic as well genes related to immune function.
2020-12-06 | GSE162721 | GEO
Project description:A functional interaction between peroxisome proliferator-activated receptor alpha (PPARalpha) and components of the circadian clock has been suggested; however, it remains to be clarified whether those transcriptional factors interact with each other to regulate the expression of their target genes. In this study, we used a ligand of PPARalpha, bezafibrate, to search the PPARalpha-regulated genes that express in a CLOCK-dependent circadian manner. Microarrays analyses using hepatic RNA isolated from bezafibrate treated-wild type, Clock mutant (Clk/Clk), and PPARalpha-null mice revealed that 136 genes are transcriptionally regulated by PPARalpha in a CLOCK-dependent manner.
2010-06-15 | GSE20513 | GEO
Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility.
2016-06-29 | GSE79008 | GEO
Project description:Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists have demonstrated therapeutic properties for several brain disorders, including alcohol dependence. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated and little is known about their effects in the brain. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar and fenofibrate decreased ethanol consumption in male C57BL/6J mice while bezafibrate did not. Hypothesizing that fenofibrate and tesaglitazar are causing brain gene expression changes that precipitate the reduction in ethanol drinking, we gave daily oral injections of fenofibrate, tesaglitazar and bezafibrate to mice for eight consecutive days and collected liver, prefrontal cortex and amygdala 24 hours after last injection. RNA was isolated and purified using MagMAX-96 Total RNA Isolation Kit. Biotinylated, amplified cRNA was generated using Illumina TotalPrep RNA Amplification Kit and hybridized to Illumina MouseWG-6 v2.0 Expression microarrays. Mice were divided into four groups (N=10 per group): fenofibrate, tesaglitazar, bezafibrate and saline. See summary and protocols for details.
2015-04-14 | E-GEOD-67796 | biostudies-arrayexpress
Project description:We found that bezafibrate, PPAR-alpha agonist, increased EEG delta oscillation throughout 24 hours and decreased body temperature especially in the later half of the dark period in mice. This DNA- microarray experiment was performed due to investigate the gene expression at ZT10, when body temperature showed no difference between nomal- and bezafibrate-treated mice, and ZT22, when body temperature showed the largest difference between the groups. Keywords: drug treatment, time course
2008-08-01 | GSE10417 | GEO
Project description:Gene expression data of bezafibrate treated CD8+ T cells
| PRJNA486360 | ENA
Project description:Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that act as ligand-activated transcription factors. Although prescribed for dyslipidemia and type-II diabetes, PPAR agonists have demonstrated therapeutic properties for several brain disorders, including alcohol dependence. PPAR agonists decrease ethanol consumption and reduce withdrawal severity and susceptibility to stress-induced relapse in rodents. However, the cellular and molecular mechanisms facilitating these properties have yet to be investigated and little is known about their effects in the brain. We tested three PPAR agonists in a continuous access two-bottle choice (2BC) drinking paradigm and found that tesaglitazar and fenofibrate decreased ethanol consumption in male C57BL/6J mice while bezafibrate did not. Hypothesizing that fenofibrate and tesaglitazar are causing brain gene expression changes that precipitate the reduction in ethanol drinking, we gave daily oral injections of fenofibrate, tesaglitazar and bezafibrate to mice for eight consecutive days and collected liver, prefrontal cortex and amygdala 24 hours after last injection. RNA was isolated and purified using MagMAX-96 Total RNA Isolation Kit. Biotinylated, amplified cRNA was generated using Illumina TotalPrep RNA Amplification Kit and hybridized to Illumina MouseWG-6 v2.0 Expression microarrays.
2015-04-14 | GSE67796 | GEO