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ABSTRACT: Nanotherapy for MCD induced NASH model

PROVIDER: PRJNA981653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24880839_1.fastq.gz	Fastqsanger.gz
	SRR24880839_2.fastq.gz	Fastqsanger.gz
	SRR24880840_1.fastq.gz	Fastqsanger.gz
	SRR24880840_2.fastq.gz	Fastqsanger.gz
	SRR24880841_1.fastq.gz	Fastqsanger.gz

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Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.

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Project description:Kupffer cells (KCs) self-renew by local proliferation in the adult independently from monocytes (Mos). However, how they maintain during chronic metabolic disorders such as non-alcoholic steatohepatitis (NASH) remains ill-defined. We characterized KCs during NASH and observed diversity in the KC pool, with a significant fraction of monocyte-derived KCs (MoKCs). Here, we aim to uncover the transcriptional landscapes of KCs subsets found in a mouse model of methionine and choline deficient (MCD)-diet induced non-alcoholic steatohepatitis (NASH).

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and MttpIKO liver Transcriptomes on methioine defcient diet (MCD)

Project description:Purpose: The goals of this study is to use NGS-derived liver transcriptome profiling (RNA-seq) to identify candidates of pathways and genes which are responsible to protect MttpIKO from MCD induced-NASH development .

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Project description:We fed control mice and Slc7a11-LTG mice methionine and Choline Deficient (MCD) to induce NASH. Whole-genome RNA sequencing were then performed in the livers of control and LTG mice fed with MCD.

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The Deubiquitinase USP28 Maintains the Expression of PPARγ and Its Inactivation Protects Mice from Diet-Induced NASH and Hepatocarcinoma

Project description:Nonalcoholic steatohepatitis (NASH), a progressive form of nonalcoholic fatty liver disease, is one of the leading causes of liver disease worldwide and may further progress to cirrhosis and cancer. However, the pathogenesis of NASH remains unclear, and there is currently only one FDA-approved drug for its treatment; therefore, new therapeutic approaches are urgently needed. Under high-fat diet or obese conditions, PPARγ is activated in the liver to promote lipid storage as droplets, inducing the progression of NASH. We showed that the expression level of USP28 is elevated in the livers of NAFLD/NASH patients. Through dietary induction, including a methionine-choline deficient (MCD) diet and a Western diet (WD) combined with intraperitoneal injection of carbon tetrachloride (CCl4), we established two severe mouse models of NASH and revealed the role of the deubiquitinase USP28. Mechanistically, the hepatic deubiquitinase USP28 directly binds to PPARγ and prevents its own ubiquitination and degradation, thereby regulating its downstream signaling pathways. In the absence of Usp28 or if the DUB is inhibited, PPARγ is downregulated, and the PPAR signaling pathway is inhibited, allowing the cells to mount a defensive response to excessive fat. Both genetic and pharmacological inactivation of Usp28 significantly attenuated the NASH phenotype induced by the MCD diet or WD-CCl4 regimen, as well as WD-CCl4-induced hepatocellular carcinoma in mice.

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Project description:To systemically investigate the mechanism underlying the impact of SOX9 on lipid metabolism in NASH, we performed RNA-seq analysis in liver tissues from Sox9HKO mice and Sox9f/f mice after 6 weeks of MCD feeding.

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