Project description:Purpose: a transcriptome analysis was used to ascertain whether lipid metabolism disorders were induced by high-fat diet (HFD), and comparisons were made between control, HFD and DfCS-Ib(treatment) groups. Methods: liver mRNA profiles of C57BL/6 mice were generated by deep sequencing using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: HFD could change the expression of some genes and disturb normal metabolisms. However, there were fewer changes for genes of DfCS-Ib group mice. According to the KEGG Pathway Database and GO analysis, genes involving in lipid biosynthesis, degradation, and transportation were changed by HFD. Conclusions: Our study indicated that DfCS-Ib alleviated lipid disorder of HFD-fed mice in liver by normalizing the expressions of related genes.
Project description:ER stress could affect many tissues, especially liver, in which non-alcoholic fatty liver disease, liver steatosis, etc. have been reported relative. But there still lack systematic insight into ER stress in liver, which can be obtained by transcriptomics of the tissue. Here, tunicamycin was utilized to induce ER stress in C57BL/6N mice. And microarray was performed to get the transcriptome alteration. Microarray of liver from tunicamycin-injected C57Bl/6N mice
Project description:C57BL/6 mice are the most widely used inbred strain for metabolic and interventional studies. It is commonly known that high-caloric diet feeding induces a heterogeneous phenotype in C57BL/6 mice similar to humans with the majority developing obesity and metabolic dysfunction whilst others remaining lean and metabolically healthy. Nevertheless, the underlying mechanism(s) for this remains unknown. Here, we show that a subset (5-25%) of all C57BL/6 mice develop spontaneous cholemia with elevated total serum bile acids and increased liver damage at early time points upon high-caloric diet feeding. Although cholemic mice are resistant to obesity and metabolic dysfunction, they develop accelerated liver damage and liver fibrosis, which ultimately predisposes them to early liver cancer compared to non-cholemic mice fed a Western-diet or choline-deficient high-fat diet. Hitherto, these mice have been overlooked, which may have led to inconsistent or perplexing findings. Therefore, C57BL/6 mice included in metabolic and cancer studies relating to the liver are strongly recommended to be screened and excluded for cholemia.
Project description:To investigate whether HBsAg intrauterine exposure affected the offspring's immune response against HBV and the relevant mechanism, the difference of fetal liver tissue transcriptome between the C57BL/6 mice and C57BL/6-Tg (HBV Alb-1) Bri44 HBV transgenic mice was analyzed.
Project description:To determine genomic sites of direct GAbpα recruitment in male C57Bl/6 mice liver tissue, we performed a cistrome analysis by chromatin immunoprecipitation using a GAbpα-specific antibody followed by massive parallel DNA sequencing (ChIP-Seq).
Project description:cDNA was prepared from total liver RNA taken from untreated, 3 months old, TLR3-/- and TLR3wt C57Bl/6 mice cDNA was prepared from total liver RNA taken from untreated, 3 months old, TLR3-/- and TLR3wt C57Bl/6 mice each group contained 3 mice
Project description:Small RNA sequencing was performed on the liver tissues of six adult female mice, including three transgenic mice with dnTGFbetaR2 and three wild-type C57BL/6 control mice. This dataset contains the raw sequencing readouts of miRNAs in the liver, which provide transcriptomic resources for studying the regulatory mechanisms mediated by miRNAs.