Effects of linoleic acid metabolite on liver gene expression in a diet-induced NAFLD/NASH model.
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ABSTRACT:
PROVIDER: PRJNA1015216 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26031775_1.fastq.gz | Fastqsanger.gz | |||
| SRR26031775_2.fastq.gz | Fastqsanger.gz | |||
| SRR26031776_1.fastq.gz | Fastqsanger.gz | |||
| SRR26031776_2.fastq.gz | Fastqsanger.gz | |||
| SRR26031777_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the alterlation of liver gene expression by linoleic acid (LA) metabolite HYA (10-hydroxy-cis-12-octadecenoic acid) in a diet-induced NAFLD/NASH model, we evaluated liver of male C57BL/6J mice fed a nomal diet (ND), a high fat diet (HFD, Control(CT)), HFD supplemented with 1% HYA (HYA), or HFD supplemented with 1% LA (LA) for 26 weeks from 5-week-old. We then performed gene expression profiling analysis using data obtained from RNA-seq of these 4 groups.
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Project description:Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is a significant risk factor for hepatocellular carcinoma (HCC). However, a preclinical model of progressive NAFLD/NASH is largely lacking. Here, we report that mice with hepatocyte-specific deletion of Tid1, encoding a mitochondrial cochaperone, tended to develop NASH-dependent HCC. Mice with hepatic Tid1 deficiency showed impairing mitochondrial function and causing fatty acid metabolic dysregulation; meanwhile, sequentially developed fatty liver, NASH, and cirrhosis/HCC in a diethylnitrosamine (DEN) induced oxidative environment. The pathological signatures of human NASH, including cholesterol accumulation and activation of inflammatory and apoptotic signaling pathways, are also present in these mice. Clinically, low Tid1 expression was associated with unfavorable prognosis in patients with HCC. Empirically, hepatic Tid1 deficiency directly disrupts entire mitochondria that play a key role in the NASH-dependent HCC development. Overall, we established a new mouse model that develops NASH-dependent HCC and provides a promising approach to improve the treatment.
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Project description:Human genetic studies have identified several MARC1 variants as protective against non-alcoholic fatty liver diseases (NAFLD). The MARC1 variants are associated with reduced lipid profiles, liver enzymes, and liver-related mortality. However, the role of mitochondrial amidoxime reducing component 1 (mARC1), encoded by MARC1, in NAFLD is still unknown and the therapeutic potential of this target has never been developed. Given that mARC1 is mainly expressed in hepatocytes, we developed an N-acetylgalactosamine conjugated mouse mARC1 siRNA to address this. In ob/ob mice, knockdown of mARC1 in mouse hepatocytes resulted in decreased liver weight, serum lipid enzymes, low-density lipoprotein cholesterol, and liver triglycerides. Loss of mARC1 also improved the lipid profiles and attenuated liver pathological changes in two diet-induced nonalcoholic steatohepatitis (NASH) mouse models. A comprehensive analysis of mARC1-deficient liver in NASH by metabolomics, proteomics, and lipidomics showed that mARC1 knockdown partially restored metabolites and lipids altered by diets. Taken together, loss of mARC1 protects mouse liver from NASH, suggesting a potential therapeutic approach of NASH by downregulation of mARC1 in hepatocytes.
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