Genome-wide RNAseq of liver tissue derived from DEN-CDA-HFD mice treated with CLDN1 mAb or vehicle Control
Ontology highlight
ABSTRACT: Seven-week old male C57BL/6J mice received a single i.p. injection of DEN (100 mg/kg) and were subsequently fed with CDA-HFD after 3 weeks. After 6 weeks of diet, the mice were randomized in 2 groups, receiving weekly i.p. injections of 500 µg of either CLDN1 specific mAb or vehicle control for 16 weeks. RNA was extracted from non-tumorous liver tissue of 6 DEN-CDA-HFD mice treated with CLDN1 mAb, 6 DEN-CDA-HFD mice treated with vehicle Control as well as 5 C57BL/6J Control mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.
Project description:Six-week old Fah−/−/Rag2−/−/Il2rg −/− (FRG) –NOD breeding mice were intravenously injected with 1.5 x 10^9 plaque forming units (pfu) of an adenoviral vector encoding the secreted form of the human urokinase-like plasminogen activator (Ad-uPA). Forty-eight hours later, 10^6 PHH were injected intrasplenically. Successfully transplanted mice were fed with CDA-HFD for 16 weeks and then treated with humanized CLDN1 specific mAb 500 µg or vehicle for additional 8 weeks. RNA was extracted from non-tumorous liver tissue of 4 NASH fibrosis mice treated with CLDN1 mAb, 3 vehicle Control treated NASH fibrosis mice as well as 3 humanized mice fed by regular diet. Libraries were sequenced on the Illumina HiSeq 4000 as Single-Read 50 base reads.
Project description:To understand the fibrotic response in the CDA-HFD induced NASH fibrosis model, we performed RNA-seq on liver samples collected from mice fed with normal chow (week 0) or CDA-HFD chow (weeks 8 and 16).
Project description:Aged (~92 weeks of age) C57BL/6J mice and young mice at 16 weeks of age were fed 60% HFD for 4 weeks containing either vehicle or 0.1% w/w BAM15. iWAT was harvested and snap frozen in liquid nitrogen. Tissue was homogenized in trizol and RNA extracted via chloroform phase separation.
Project description:Effects of EPA/DHA enriched high fat diets (HFD) compared to HFD-Corn oil after 8 weeks intervention on different adipose depots of C57BL/6J mice.
Project description:Exposure to polychlorinated biphenyls (PCBs) and high fat diet (HFD) results in nonalcoholic steatohepatitis (NASH) in mice by altering intracellular signaling and inhibiting epidermal growth factor receptor (EGFR) signaling. Post-transcriptional chemical modification (PTM) of RNA regulates biological processes. This study tested the hypothesis that PCB exposure alters the global RNA epitranscriptome in HFD-fed male mouse liver. C57BL/6J male mice were fed a 42% milk fat diet (HFD) and exposed to Aroclor 1260 (20mg/kg), PCB 126 (20 µg/kg), both Aroclor 1260 and PCB 126, or vehicle control for 12 weeks. RNA modifications altered by PCB exposure were analyzed in comparison to the readers, writers, and erasers of these marks in the RNA transcriptome.
Project description:We report the effect of NAFLD on liver gene expression changes that could impact tetrachloroethhylene metabolism Methods: We fed male C57Bl/6J mice a base diet (BD), high fat (HFD), or methionine/choline/folate deficient high fat diet (MCD) for 8 weeks and then treated them with vehicle or tetrachloroethylene (PERC, 300 mg/kg ig). We only report "basal" differences herein (aka vehicle-treated). Results: We report that there were diet-specific differences in xenobiotic metabolizing genes, and that these genes may be responsible for NAFLD-induced disruption in PERC metabolism
Project description:Male C57BL/6J mice were fed a high-fat diet (HFD, 60 kcal% fat, D12492, Research Diets, Inc) or normal standard chow diet with 10 kal% fat (ND, D09100304, Research Diets, Inc). Specifically, 6-week-old mice were fed a HFD for 12 weeks to induce insulin resistance (HFD-12w group); 14-week-old mice were fed a HFD for 4 weeks to induce obesity (HFD-4w group). Control mice were fed a ND continuously for 12 weeks starting at 6 weeks of age (ND group). All mice reached the experimental endpoint at 18 weeks of age. Insulin sensitivity was measured by glucose tolerance test and insulin tolerance test. Mice that developed insulin resistance in HFD-12w group and obese mice with normal insulin sensitivity in HFD-4w group were used for further experiments. Mice in ND group were used as controls. Upon reaching the experimental endpoint, livers from three insulin-resistant mice, three insulin-sensitive obese mice, and three control mice were removed for RNA sequencing.