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Expression data from WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hours after PHx or Sham operation

ABSTRACT: Expression data from WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hours after PHx or Sham operation

PROVIDER: PRJNA470613 | ENA |

REPOSITORIES: ENA

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Expression data from WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hours after PHx or Sham operation

Project description:PPARα act as the master of lipid metabolism in liver, however, the changes of its target genes after PHx and the effects of PPARα on regenerative genes were unknown. At 12 to 24 hours after PHx, the mice develope marked steatosis, therefore the time point of 12 hour after PHx was choosen to perform microarray analysis. We used microarray to detail the gene expression of WT (Pparafl/fl) mice and hepatocyte-specific PPARα disruption (Ppara△Hep) mice liver tissue at 12 hour after PHx or Sham operation

2018-05-10 | GSE114223 | GEO

RNA-sequence data of mouse liver sinusoidal endothelial cells on day 14 after partial hepatectomy (PHx) or sham operation

Project description:The cellular and molecular mechanisms involved in liver regeneration following partial hepatectomy (PHx) are complicated. Liver sinusoidal endothelial cells (LSECs) play key roles in orchestrating liver regeneration, especially during the inductive phase and angiogenic phase post PHx (from day 0 to day 8). However, the expression profile of LSECs during the late phase of regeneration remains poorly explored. Thus, we purified LSECs from mice underwent PHx or sham operation at day 14 to unravel their transcriptome changes in the late phase of liver regeneration.

2021-08-06 | GSE181482 | GEO

mRNA sequencing of the mouse and human Hep-Orgs, Chol-Orgs and primary hepatocytes

Project description:The mammalian liver possesses a remarkable regenerative ability. 1) The 'oval cell' response emanates from the biliary tree when all hepatocytes are affected by chronic liver disease. 2) A massive, proliferative response of mature hepatocytes occurs upon acute liver damage such as partial hepatectomy (PHx). We establish a long-term 3D organoid culture system from mouse and human fetal/pediatric/adult hepatocytes that retain key morphological and functional features of hepatocytes fate. We report the mRNA and single cell sequencing of Hep-Orgs from different donors in different passages. We compared Hep-Orgs with primary hepatocytes, proliferative hepatocytes or Chol-Orgs derived from Epcam+ biliary cells. By analyzing, we determine similar gene expression profile of Hep-Orgs with primary hepatocytes and make genes lists distinguished with undamaged hepatocytes as well. We find the Hep-Orgs resemble proliferative damage-response of hepatocytes after partial hepatectomy while Chol-Orgs express high cholangiocytes markers. The sequencing data constitutes a valuable resource to understand liver organoids especially Hep-Orgs.

2018-11-29 | GSE111301 | GEO

Characterize osteocyte transcriptome under control of PPARa

Project description:RNA-seq analysis of transcriptome of osteocytes isolated from femora cortical bone of 5 mo old C57BL6 mice with WT or PPARa KO genotype. Conclusion: In osteocytes, PPARα controls large number of transcripts coding for signaling proteins and osteocyte secretome which regulates development of bone marrow adipose tissue and peripheral fat metabolism.

2023-03-28 | GSE225595 | GEO

Expression profiling in liver of wild type and Ppara-null mice treated with PPARA agonists [RNA-seq]

Project description:To clarify the mechanism underlying the proliferation of hepatocytes induced by PPARA agonists, expression profiling in liver of wild type and Ppara-null mice treated with PPARA agonist was investigated.

2022-04-05 | GSE154275 | GEO

PPARα mouse liver cistrome

Project description:Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1-3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPARα and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPARα reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARα knockout (PPARα-/-) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR-/-) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARα and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. Mouse liver PPARα cistromes in fed 8-week-old male WT or PPARα KO mice treated with or without its synthetic agonist ligand GW7647twice a day were generated by deep sequencing in quadruplicate using illumina

2014-09-27 | E-GEOD-61817 | biostudies-arrayexpress

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

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

Real-time quantitative PCR analysis of fatty acid metabolism genes of liver tissue from wild-type and PPARa (-/-) mice exposed to 2,4-dinitrotoluene (PPARa)

Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice. RNA was isolated from liver tissue of vehicle or 2,4-DNT treated wild-type or PPARα (-/-) mice (n=6) and RT-PCR performed to analyze genes involved in fatty acid metabolism

2014-06-30 | E-GEOD-50167 | biostudies-arrayexpress

Genome-wide profiling of PPARA in PPARA agonist-treated mouse livers [ChIP-seq]

Project description:To clarify mouse PPARA autoinduction and hepatocyte proliferation signaling pathways, genome-wide distribution of PPARA in the liver of PPARA agonist-treated mice compared to Vehicle was analyzed.

2022-04-05 | GSE154276 | GEO

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