Gene expression data of bezafibrate treated CD8+ T cells
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ABSTRACT:
PROVIDER: PRJNA486360 | ENA |
REPOSITORIES: ENA
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Project description:Activation of PPAR by bezafibrate synergize with PD-1 blockade. We found that PPAR activation enhanced the anti-apoptotic property of CD8+ T cells and increased its number in tumor site. PPAR target genes includes various genes associated with metabolic pathways. Using the microarray assay we found that fatty acid oxidation related genes and immune function related genes are involved in the enhnacement of antitumor immunity. Microarrays have been used to identify the genes, which include metabolic as well genes related to immune function, regulated by PPAR activation.
2018-08-17 | GSE118659 | 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. 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: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. 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: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
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