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Liver expression data from four mouse strains treated with vehicle or PF-04287881 for seven days

ABSTRACT: PF-04287881 induced varying degrees of liver necrosis and phospholipidosis in a 34-inbred strain Mouse Diversity Panel (MDP) study. Four strains with differing susceptibilities to these phenotypes (MA/MyJ, NZW/LacJ, SM/J, WSB/EiJ) were selected for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive PF-04287881-induced liver injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE52620 | GEO | 2016/10/21

SECONDARY ACCESSION(S): PRJNA229488

REPOSITORIES: GEO

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Liver expression data from four mouse strains treated with vehicle or PF-04287881 for seven days

Project description:PF-04287881 induced varying degrees of liver necrosis and phospholipidosis in a 34-inbred strain Mouse Diversity Panel (MDP) study. Four strains with differing susceptibilities to these phenotypes (MA/MyJ, NZW/LacJ, SM/J, WSB/EiJ) were selected for analysis of gene expression changes in the liver. The objective of this study was to identify gene expression changes that drive PF-04287881-induced liver injury. Thirty-one total samples were analyzed: N=4 per treatment and strain, except PF-04287881-treated WSB/EiJ (N=3) where one animal died before the completion of the study due to gavage error. Two strains exhibited findings of PF-04287881-induced Kupffer cell vacuolation and were coded as phospholipidosis responders (MA/MyJ and NZW/LacJ). One strain exhibited findings of single cell necrosis and was coded as a necrosis responder (NZW/LacJ).

2016-10-21 | E-GEOD-52620 | biostudies-arrayexpress

Allele-specific expression in liver, hypothalamus and vomeronasal organ of Mus.m.musculus and M.m. domesticus

Project description:We performed RNaseq of liver, hypothalamus and vomeronasal organ crosses between inbred stains of M. m. domesticus (strain WSB/EiJ) and M. m. musculus (PWD/PhJ). We also sequenced RNA from the same tissues from parental M. m. musculus (PWD/PhJ).

2015-02-10 | E-MTAB-3288 | biostudies-arrayexpress

Testis expression in Mus musculus domesticus WSB/EiJ x Mus musculus musculus PWD/PhJ F2 hybrids

Project description:To characterize the genetic basis of hybrid male sterility in detail, we used a systems genetics approach, integrating mapping of gene expression traits with sterility phenotypes and QTL. We measured genome-wide testis expression in 305 male F2s from a cross between wild-derived inbred strains of M. musculus musculus and M. m. domesticus. We identified several thousand cis- and trans-acting QTL contributing to expression variation (eQTL). Many trans eQTL cluster into eleven M-bM-^@M-^Xhotspots,M-bM-^@M-^Y seven of which co-localize with QTL for sterility phenotypes identified in the cross. The number and clustering of trans eQTL - but not cis eQTL - were substantially lower when mapping was restricted to a M-bM-^@M-^XfertileM-bM-^@M-^Y subset of mice, providing evidence that trans eQTL hotspots are related to sterility. Functional annotation of transcripts with eQTL provides insights into the biological processes disrupted by sterility loci and guides prioritization of candidate genes. Using a conditional mapping approach, we identified eQTL dependent on interactions between loci, revealing a complex system of epistasis. Our results illuminate established patterns, including the role of the X chromosome in hybrid sterility. Gene expression was measured in whole testis in males aged 70(M-BM-15) days. Samples include 294 WSB/EiJ x PWD/PhJ F2s, 11 PWD/PhJ x WSB/EiJ F2s, 8 WSB/EiJ, 8 PWD/PhJ, 6 PWD/PhJ x WSB/EiJ F1s and 4 WSB/EiJ x PWD/PhJ F1s.

2014-05-01 | E-GEOD-54089 | biostudies-arrayexpress

Candidate Gene Identification Through RNA-Seq Analysis of (TRAMP x WSB/EiJ) F2 Primary Tumors

Project description:RNA-seq analysis of 115 randomly selected (TRAMP x WSB/EiJ) F2 prostates that had been harvested at experimental termination was performed to identify metastasis associated transcriptomic changes

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Interstrain differences in the severity of liver injury induced by a choline- and folate-deficient diet in mice are associated with dysregulation of genes involved in lipid metabolism.

Project description:Nonalcoholic fatty liver disease (NAFLD) is a major health problem and a leading cause of chronic liver disease in the United States and developed countries. In humans, genetic factors greatly influence individual susceptibility to NAFLD. The goals of this study were to compare the magnitude of interindividual differences in the severity of liver injury induced by methyl-donor deficiency among individual inbred strains of mice and to investigate the underlying mechanisms associated with the variability. Feeding mice a choline- and folate-deficient diet for 12 wk caused liver injury similar to NAFLD. The magnitude of liver injury varied among the strains, with the order of sensitivity being A/J M-bM-^IM-^H C57BL/6J M-bM-^IM-^H C3H/HeJ < 129S1/SvImJ M-bM-^IM-^H CAST/EiJ < PWK/PhJ < WSB/EiJ. The interstrain variability in severity of NAFLD liver damage was associated with dysregulation of genes involved in lipid metabolism, primarily with a down-regulation of the peroxisome proliferator receptor M-NM-1 (PPARM-NM-1)-regulated lipid catabolic pathway genes. Markers of oxidative stress and oxidative stress-induced DNA damage were also elevated in the livers but were not correlated with severity of liver damage. These findings suggest that the PPARM-NM-1-regulated metabolism network is one of the key mechanisms determining interstrain susceptibility and severity of NAFLD in mice. Male A/J, C3H/HeJ and WSB/EiJ inbred mice were maintained on either control or choline- and folate-deficient (CFD) diets for 12 weeks. Gene expression profiles in the livers from control mice and mice fed a CFD-diet were investigated.

2014-10-16 | E-GEOD-62362 | biostudies-arrayexpress

Effect of PF-429242 on gene expression in liver cancer cells

Project description:To analyze the PF-429242-induced gene expression changes in PLC/PRF/5 and HepG2 liver cancer cells.

2023-10-22 | GSE228257 | GEO

A neuroprotective locus modulates ischemic stroke infarction independent of collateral vessel anatomy

Project description:The strains, C57BL6/J, C3H/HeJ, and WSB/EiJ, show a similar collateral vessel anatomy but differ infarct volume after ischemic stroke induction. To identify a gene(s) exhibiting differential gene expression, we performed RNA seq experiment within these mouse strains.

2021-03-06 | GSE168383 | GEO

Expression data from livers of high fat fed rats treated with ACC inhibitor PF-04923503

Project description:Fundamental alterations in lipid metabolism including increased rates of de novo lipogenesis (DNL), reduced fatty acid oxidation (FAOX) and ectopic lipid accumulation in skeletal muscle and liver are characteristic of type 2 diabetes mellitus (T2DM) and have been hypothesized to directly contribute to the molecular pathogenesis of the disease. Acetyl-CoA carboxylase (ACC) catalyzes the formation of malonyl-CoA, the rate limiting substrate for DML and key regulator of FAOX. ACC inhibitors have the potential to pharmacologically rebalance these metabolic alterations. In the present study, PF-04923503, a potent dual ACC1/ACC2 inhibitor with properties optimized for in vivo studies, suppressed levels of malonyl-CoA in primary hepatocytes, rat skeletal muscle ex vivo, as well as rat liver and skeletal muscle in vivo. This impact on malonyl-CoA was directly correlated (r2>0.9) with reduced hepatic DNL and inversely correlated with incresed rates of FAOX (r2>0.9). The pharmacological eccfect of PF-04923503 persisted with chronic treatment. High-fat fed rats treated with PF-04923503 for six weeks showed dose-dependent reductions in skeletal muscle and liver lipid accumulation. These changes correlated directly with markers for improved insulin sensitization. However, liver gene expression indicates that pharmacological inhibition results in compensation by up-regualtion of genes involved with DNL. These results suggest that pharmacological inhibition of ACC may have utility to help rebalance metabolic abnormalities in T2DM and improve insulin sensitivity. Differential gene expression was assessed by Affymetrix microarray experiments for 15 liver samples across 3 pharmacological treatment groups (vehicle control 0.5% methylcellulose had 5 samples, PF-04923503 10mpk had 5 samples, PF-04923503 30mpk had 5 samples)

2011-06-30 | E-GEOD-28058 | biostudies-arrayexpress

Transcriptomic Profiling of Collaborative Cross Founder Mouse Embryonic Fibroblasts stimulated with Type I, II and III Interferons

Project description:Collaborative Cross (CC) mouse embryonic fiborolasts (MEF) cells obtained from the eight Founder animals [PWK/PhJ, NZO/HILtJ, NOD/ShiLtJ, WSB/EiJ, A/J, CAST, C57BL/6J, and 129/SvlmJ] were immortalized and the cell lines used to assess differences in transcriptional responses following treatment with type I, II and III recombinant mouse interferon.

2014-05-27 | GSE53057 | GEO

Interstrain differences in the severity of liver injury induced by a choline- and folate-deficient diet in mice are associated with dysregulation of genes involved in lipid metabolism.

Project description:Nonalcoholic fatty liver disease (NAFLD) is a major health problem and a leading cause of chronic liver disease in the United States and developed countries. In humans, genetic factors greatly influence individual susceptibility to NAFLD. The goals of this study were to compare the magnitude of interindividual differences in the severity of liver injury induced by methyl-donor deficiency among individual inbred strains of mice and to investigate the underlying mechanisms associated with the variability. Feeding mice a choline- and folate-deficient diet for 12 wk caused liver injury similar to NAFLD. The magnitude of liver injury varied among the strains, with the order of sensitivity being A/J ≈ C57BL/6J ≈ C3H/HeJ < 129S1/SvImJ ≈ CAST/EiJ < PWK/PhJ < WSB/EiJ. The interstrain variability in severity of NAFLD liver damage was associated with dysregulation of genes involved in lipid metabolism, primarily with a down-regulation of the peroxisome proliferator receptor α (PPARα)-regulated lipid catabolic pathway genes. Markers of oxidative stress and oxidative stress-induced DNA damage were also elevated in the livers but were not correlated with severity of liver damage. These findings suggest that the PPARα-regulated metabolism network is one of the key mechanisms determining interstrain susceptibility and severity of NAFLD in mice.

2014-10-16 | GSE62362 | GEO

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