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Liver Transcriptomes of Simple steatosis in Mice

ABSTRACT: Liver Transcriptomes of Simple steatosis in Mice

PROVIDER: PRJNA818539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18429500_1.fastq.gz	Fastqsanger.gz
	SRR18429500_2.fastq.gz	Fastqsanger.gz
	SRR18429501_1.fastq.gz	Fastqsanger.gz
	SRR18429501_2.fastq.gz	Fastqsanger.gz
	SRR18429496_1.fastq.gz	Fastqsanger.gz

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Liver Transcriptomes of Simple steatosis in Mice

Project description:In our study, we constructed a Simple steatosis (NAFL) mouse model with a high-fructose and high-cholesterol (HFHC diet) for 12 weeks. Next, we performed RNA Sequencing analysis to reveal molecular features of Simple steatosis. As a result, we obtained hepatic genome-wide mRNA expression in the livers from two groups of mice (NAFL versus Normal).Using FDR < 0.01 and fold change > 2 as the threshold, we identified 176 differentially expressed genes (DEGs) in the livers of NAFL mice relative to the normal control mice, of which 118 up-regulated and 58 down-regulated. The top 5 up-regulated genes in NAFL mice included the genes encoding for Themis, Cfd, Aqp8, Osbpi3 and Scd1.

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Characteristics of liver tissues of MASH compared to those of Simple Steatosis mice.

Project description:Characteristics of hepatocytes of Metabolic Dysfunction-Associated Steatohepatitis (MASH) mice were compared compared to those of Simple Steatosis (SS) mice in the context of UPR response.

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Proteomic Profile Analysis of Simple steatosis and Non-alcoholic Steatohepatitis in Mice

Project description:Through mass spectrometry, we quantified liver global proteomes of Simple steatosis and Non-alcoholic Steatohepatitis in a HFHC diet induced mouse model

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Hepatocyte-specific Angiotensinogen Deficiency Inhibits Western Diet-induced Liver Steatosis With Suppression of Cell Division in Mice

Project description:Liver steatosis is a common cause of chronic liver disease. To investigate the molecular basis of hepatic steatosis, low-density lipoprotein receptor-deficient (LDLR -/-) mice were fed Western diet (WD, 42% of calories from fat) for 5, 14, or 42 days and evaluated against mice fed a normal laboratory diet. Histological analyses revealed that steatosis was detected as early as 14 days of WD feeding. Bulk RNA sequencing demonstrated that WD feeding altered liver transcriptomes related to inflammation and cell adhesion consistent with the progression of liver steatosis. Previous studies determined that hepatocyte-specific deficiency of angiotensinogen (AGT), the unique substrate of the renin-angiotensin system (RAS), alleviates WD-induced hepatic steatosis in mice. However, the effects of hepatic AGT deficiency were not mimicked by pharmacological inhibition of the RAS, and the molecular mechanisms by which AGT deficiency protects against WD-induced steatosis is unknown. Therefore, liver transcriptomes were compared between hepatocyte-specific AGT deficient mice (hepAGT -/-) and their wild-type littermates (hepAGT +/+) after 14 days of WD feeding. Gene ontology analyses showed that upregulated genes in hepAGT -/- mice were enriched for metabolic processes and downregulated genes were enriched for cell division pathways. The integration analysis of the two RNA sequencing data identified 5 key genes, Smpd3, Dtl, Cdc6, Mki67, and Top2a, which were primarily associated with cell division processes in hepAGT +/+ mice and were suppressed in hepAGT -/- mice. In conclusion, hepatic AGT deficiency downregulated genes related to cell division during the progression of liver steatosis.

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Project description:In our study, C57BL/6 male mice were fed a normal chow diet or high-fat diet additionally containing high-fructose and high-cholesterol (HFHC diet) for 12 weeks and 28 weeks to construct simple steatosis (NAFL) and Non-alcoholic steatohepatitis (NASH) models respectively. Through lncRNA sequencing, a total of 1131 lncRNAs (798 up-regulated and 333 down-regulated) and 5161 lncRNAs (3168 up-regulated and 1993 down-regulated) were differentially expressed in livers of NAFL and NASH mice respectively. A total of 614 lncRNAs (455 up-regulated and 159 down-regulated) were dysregulated in both NASH and NAFL mice, while 4547 lncRNAs (2713 up-regulated; 1834 down-regulated) were altered specifically in NASH mice.

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