ABSTRACT: Expression data from mouse livers of control mice (RECS1-flox) and hepatocyte specific RECS1 deficiency mice (RECS1-HKO) after fed with HFD for 8 weeks
Project description:Purpose: The goal of this study is to compare transcriptome profilings of liver from Mettl3 flox/flox and hepatocyte-specific Mettl3 knockout (HKO) mice. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from livers of Mettl3 flox/flox and HKO mice at 8 weeks old. mRNA profiles were generated by deep sequencing using an Illumina HiSeq X Ten platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.90) with Hisat2 (version 2.0.4), and the aligned reads were used to quantify mRNA expression by using HTSeq (version 0.9.1). Conclusion: The hepatic mRNA profiles in Mettl3 flox/flox and HKO mice were characterized.
Project description:To investigate the potential mechanism by which RECS1 regulate metabolic disorder, we treated control mice and RECS1 HKO mice with HFD for 8 weeks, and performed microarray to identify the expression pattern and the potential important molecules regulated by RECS1. We used microarrays to detect the global gene expression in the livers of control mice and RECS1 HKO mice after treatment with HFD for 8 weeks and identified distinct classes of altered genes in the livers of mice upon HFD compared .
Project description:ionPurpose: The goal of this study is to investigate how HuR regulates NASH progression. Methods: The hepatic mRNA profiles of HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice (n=3 for each group) fed with an MCD for 3 weeks were generated by deep sequencing using an Illumina Novaseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.p6) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of hepatic mRNA profiles in HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice fed with an MCD for 3 weeks, generated by RNA-seq technology. Our results show that 353 genes were upregulated and 422 genes were downregulated. Gene Ontology (GO) analysis showed that genes related to leukocyte migration, leukocyte chemotaxis, cell chemotaxis, neutrophil migration and Fc receptor signaling pathway were significantly decreased, which contributes to the protective effects of NASH progression in HKO mice.
Project description:Purpose: The goal of this study is to compare transcriptome profilings of liver from Wtapflox/flox and hepatocyte-specific Wtap knockout (HKO) mice. Methods: Total RNA was extracted using Tripure Isolation Reagent (Roche, Mannheim, Germany) from livers of Wtap flox/flox and Wtap-HKO mice at 8 weeks old. mRNA profiles were generated by deep sequencing using an Illumina Novaseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.p6) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of hepatic mRNA profiles in Wtapflox/flox and Wtap-HKO mice at 8 weeks old, generated by RNA-seq technology. Our results showed that 3486 genes were downregulated, and 3706 genes were upregulated. Gene ontology (GO) analysis showed that downregulated genes were associated with small molecule catabolic process, fatty acid metabolic process, amino acid metabolic process, steroid metabolic process, cholesterol metabolic process, xenobiotic metabolic process, fatty acid beta-oxidation, alcohol metabolic process, and glucose metabolic process, whereas the upregulated genes were associated with wound healing, leukocyte migration, chemotaxis, and positive regulation of cytokine production.
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.
Project description:Purpose: RNAseq analyses were conducted to screen for the genes undergoing transcriptional changes either in the liver of high-fat-diet (HFD)-induced obese mice or in the liver of Lepr-deficient db/db mice compared to the livers of the respective control mice Methods: C57BL/6 wild-type male mice were fed on high-fat diet (HFD) or a low-fat diet (NCD) for 18 weeks starting from 6 weeks of age, and the livers were collected at 24 weeks of age at ad libitum-fed condition.Misty/misty or db/db were sacrificed at ad libitum-fed condition at 10weeks and the liver was collected. Results: 2079 genes and 1085 genes were identified in high-fat-diet fed mice and db/db mice, respectively.
Project description:Adult PPARg floxed male and female mice were fed a high fat diet (HFD) for 16 weeks to induce obesity. Half of these mice were then injected with AAV8-TBG-Cre to knockout PPARg in hepatocytes. The remaining half were injected with AAV8-TBG-Null to generate control mice. After two weeks, mice fed the HFD were either maintained on this diet or switched to a high fat, high cholestrol, high fructose (HFCF) diet for an additional 16 weeks. This study was designed to examine whether the loss of hepatocyte PPARg in mice with established obesity would alter the liver transcriptomics in a PPARg dependent manner when the mice are fed a HFD or a HFCF diet.
Project description:This study sought to interrogate the effects of lipids and lipid metabolites on the hepatic proteome. Protein expression in high-fat diet (HFD) mouse livers vs. livers of normal chow fed (NC) mice were investigated using multiplexed quantitative LC-MS/MS (TMT labeling). This experiment contains additional replicates for normal chow and mice on high-fat diet for 16 weeks.
Project description:We mapped the genome-wide profiles of Histone H3K27 acetylation (two time points, ZT0 and ZT12) by using ChIP-Seq in livers from control mice and mice fed High Fat Diet (HFD) for 12 weeks
Project description:LASS2 is expressed mostly in human liver. We explored roles of LASS2 in pathogenesis of hepatic steatosis. Hepatocyte-specific LASS2 knockout (LASS2-/-) mice were generated using Cre-LoxP system. LASS2-/- and wild-type (WT) mice were fed with chow or high-fat diet (HFD). We performed global gene expression analysis for the mice livers in accordance with standard Affymetrix protocols to explore signaling pathways involved by LASS2 deficiency.
