Project description:Lysosome-enriched fractions from the liver of Cln8 KO mice and WT mice. Included are four datasets: 1. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 1 (CLN8_KO_1). 2. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 2 (CLN8_KO_2). 3. Lysosome-enriched fraction from the liver of WT mice, replicate 1 (WT_1). 4. Lysosome-enriched fraction from the liver of WT mice, replicate 2 (WT_2).
Project description:This experiment consists of RNAseq of liver harvested from CDAHFD mice treated for 8 weeks with either the MGAT2 inhibitor compound BMS-963272 (N = 10) or with vehicle (N = 10).
Project description:This experiment consists of RNAseq of liver harvested from CDAHFD mice treated for 8 weeks with either the MGAT2 inhibitor compound BMS-963272 (N = 10) or with vehicle (N = 10).
Project description:We generated genome-wide cistromes of BAF180 subunit of the SWI-SNF chromatin remodeling complex in mouse liver at CT10 and CT22. In addition, we performed ChIP-Seq analysis on REV-ERBα in WT and SRC-2-/- mouse liver at CT10. We found circadian oscilation of BAF180 chromatin recruitment in mouse liver with peak recruitment at CT22 and nadir at CT10. Further,REV-ERBα chromatin recruitment was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10. ChIP-Seq for BAF180 was performed in WT mice liver at CT10 and CT22 using two different antibodies. ChIP-Seq for REV-ERBα was performed in WT and SRC-2-/- mice in liver at CT10 with biological replicates.
Project description:We futher characterized genome-wide chromatin accessibility of WT and SRC-2-/- mouse liver at CT10 through DNase-Seq. In addition,chromatin accessibility was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10. DNase-Seq was carried out in WT and SRC-2-/- mice in liver at CT10 using two doses of DNaseI.
Project description:This SuperSeries is composed of the following subset Series:; GSE11940: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Doxorubicin study; GSE11941: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Trovafloxacin study Experiment Overall Design: Refer to individual Series
Project description:We reported the liver XBP1s cistrome (taken at 4h interval for a total of 48 hrs) in the liver of wild-type mice and XBP1 liver-specific knockout mice
Project description:Background
Carnitine O-octanoyltransferase (CROT) is a well-established peroxisomal enzyme involved in liver fatty acid oxidation, but less is known about its recently discovered role in promoting vascular calcification, and whether CROT-dependent liver metabolism contributes to the latter. To date, CROT function in the context of calcification potential has been conducted in the dyslipidemic low-density lipoprotein receptor-deficient (Ldlr-/-) mice.
Methods and Results
To differentiate peroxisome and CROT-dependent lipid biology from that of lipoprotein-mediated lipid biology, we therefore conducted a metabolomic analysis of the liver and plasma of normolipidemic CROT-deficient (Crot-/-) mice. We performed LC-MS-based metabolomics on liver and plasma derived from Crot-/- and Crot+/- mice and sibling Crot+/+ mice, using a dual-phase metabolite extraction protocol, and multiple LC-MS acquisition strategies. We identified between 79 to 453 annotated metabolites from liver samples, and 117 to 424 annotated metabolites from plasma samples. Through differential abundance analysis, we determined that omega-3 fatty acids such as EPA, DPA, and DHA were higher in the liver of Crot-/- and Crot+/- mice than Crot+/+ mice. EPA were higher in plasma of Crot-/- mice than Crot+/+ mice. We also determined that the anti-inflammatory dicarboxylic acids, tetradecanedioic acid and azelaic acid, were higher in the plasma of CROT-deficient mice.
Conclusions
Our study associated genetic CROT deletion with increased levels of anti-inflammatory molecules in mouse liver and plasma. These results suggest a potential mechanism for anti-calcification effects of CROT suppression and the potential use of omega-3 fatty acids as biomarkers for future CROT inhibition therapies.