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Gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

ABSTRACT: Gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

PROVIDER: PRJNA547791 | ENA |

REPOSITORIES: ENA

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Gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

Project description:Gene expression in adult male mouse liver was assayed by RNA-seq, as part of a study of liver transcriptomic changes in response to activation of PPARA by WY-14643.

2020-09-14 | GSE132386 | GEO

Impact of Gm15441 knockdown on gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

Project description:Gene expression in livers of wild type adult male mice and in Gm15441 knockdown adult male mouse liver (Gm15441-LSL mice) was assayed by RNA-seq, as part of a study of liver transcriptomic changes in response to activation of PPARA by WY-14643.

2020-09-14 | GSE132385 | GEO

RNA-sequencing of control and wy-14643 treated livers in wt and sirt6-hz mice

Project description:wy-14643 activates PPARA to promote beta oxidation. SIRT6 is known to promote beta oxidation. Here we examine the effect of PPARA activation in SIRT6 heterozygote mice.

2019-12-15 | GSE140063 | GEO

Impact of knockdown of the lncRNA 3930402G23Rik on gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

Project description:Gene expression in livers of wild type adult male mice and in lncRNA 3930402G23Rik ("G23Rik") knockdown adult male mouse liver was assayed by RNA-seq, as part of a study of liver transcriptomic changes in response to activation of PPARA by WY-14,643, published in Molecular and Cellular Endocrinology (2022). These studies found that G23Rik-null mice were more susceptible to hepatic lipid accumulation in response to acute fasting. Histological analysis further revealed a pronounced buildup of lipid droplets and a significant increase in neutral triglycerides and lipids as indicated by enhanced oil red O staining of liver sections. Hepatic cholesterol, non-esterified fatty acid, and triglyceride levels were significantly elevated in G23Rik-null mice and associated with induction of the lipid-metabolism related gene Cd36. These findings provide evidence for a lncRNA dependent mechanism by which PPARA attenuates hepatic lipid accumulation in response to metabolic stress through lncRNA G23Rik induction.

2022-07-31 | GSE197885 | GEO

Impact of Gm15441 knockdown on gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

Project description:Impact of Gm15441 knockdown on gene expression profile of mouse liver in response to activation of PPARA by WY-14643.

| PRJNA547784 | ENA

Effect of WY-14643 on Rat Primary Hepatocytes.

2012-08-28 | GSE40346 | GEO

Gene expression profile in livers from control or Wy-14643 treated MycF/F or MycF/F,ERT2-Cre mice

Project description:Genes responsible for the effects of PPARalpha agonist Wy-14643 on liver

2013-01-30 | GSE43842 | GEO

Gene expression profile in livers from control or Wy-14643 treated MycF/F or MycF/F,ERT2-Cre mice

Project description:Genes responsible for the effects of PPARalpha agonist Wy-14643 on liver 4 groups were included, MycF/F+ con, MycF/F+ Wy, MycF/F, ERT2-Cre+ Con, MycF/F,ERT2-Cre+Wy

2013-01-30 | E-GEOD-43842 | biostudies-arrayexpress

Effect of WY-14643 on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with WY-14643 treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses 8 uM and 200 uM) of WY-14643 and 1% DMSO vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis. This series is part of a SuperSeries in which primary rat hepatocytes were treated with two doses of ten chemical compounds (and corresponding vehicle controls) for 24 and 48 hours. Each compound/vehicle treatment group was an individual study performed at different times. Each study was analyzed separately and themes common between studies were reported. Time Course/Dose Response

2012-08-28 | E-GEOD-40346 | biostudies-arrayexpress

Resistance to thyroid hormone (RTH) and PPARa activation

Project description:In this study we used the d337T TRb transgenic mouse that has been created to reproduce the human genetic disease known as resistance to thyroid hormone (RTH) as a model to determine if the d337T TRb mutation would have an effect on PPARa activation. A single amino acid deletion (d337T) abrogates thyroid hormone (T3) binding and transforms the thyroid hormone receptor (TRb) into a constitutive repressor. The principle goal was to determine if T3 regulates myocardial energy metabolism through its nuclear receptors. We introduced a known PPARa activator (WY14, 643) into control and d337T TRb transgenic mice then examined cardiac gene expression using Affymetrix 430_2 expression arrays and RT-PCR. We compared the gene expression of PPARa, RXRb and TRa,b and three PPARa target genes among four studies groups [control, control with WY14, 643, d337T TRb, and d337T TRb with WY14, 643] consisting of seven mice per group. Microarray analysis revealed that these genes responded to the WY14, 643 treatments of control and d337T TRb mice. Analysis of the array and RT-PCR data indicates that mRNA expression levels of PPARa and mRXRb decrease after a six hour drug treatment in both control and d337T TRb mice (P<0.01) as did the array mRNA expression levels for TRa & b (P<0.025). Three target genes (AMPD3, PDK4 and UCP3) of PPARa were up regulated in control and down regulated in the d337T TRb transgenic mouse, indicating a direct action on these metabolic genes when the TRb becomes a repressor. In conclusion, PPARa activation by WY14, 643 has a positive effect on control mice and a negative effect on the TRb transgenic mice which supports our hypothesis that T3 regulates myocardial energy metabolism through its nuclear receptors. Keywords: treatment and deletion effects

2005-09-26 | GSE3067 | GEO

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