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Whole-genome transcritome analysis of diet-induced murine NASH

ABSTRACT: Whole liver from mice with diet-induced nonalcoholic fatty liver disease (NASH) was subjected to bulk RNA-seq. Ingenuity pathway analysis implicated pathways related to the leukocyte adhesion and differentiation in the pathogenesis of NASH. Among the adhesion molecules expressed in endothelial cells, only Icam1 (Log2FC: 1.99; FDR: 1.55E-37) and Vcam1 (Log2FC: 1.93; FDR: 9.32E-35) were differentially upregulated in NASH liver.

ORGANISM(S): Mus musculus

PROVIDER: GSE164084 | GEO | 2021/02/01

REPOSITORIES: GEO

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Genome-wide transcriptome analysis of liver sinusoidal endothelial cells in the pathogenesis of NASH

Project description:We isolated liver sinusoidal endothelial cells (LSEC) from mice fed control chow (Chow) or the nonalcoholic steatohepatitis (NASH)-inducing high fat, fructose and cholesterol (FFC) diet, and subjected the cells to bulk RNA-seq. Out of 13993 transcripts detected, the adhesion molecule Vcam1 was significantly upregulated in LSEC from FFC-fed mice compared to Chow-fed mice (Log2FC: 0.925, p: 3.6x10E-18), whereas the upregulation of another adhesion molecule Icam1 (Log2FC: 0.416, p: 0.014) was not as striking as Vcam1.

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Genome-wide open chromatin analysis of liver sinusoidal endothelial cells in the pathogenesis of NASH

Project description:We isolated liver sinusoidal endothelial cells (LSEC) from mice fed control chow (Chow) or the nonalcoholic steatohepatitis (NASH)-inducing high fat, fructose and cholesterol (FFC) diet, and subjected the cells to Omni-ATAC-seq. Out of the top 500 differentially abundant open chromatin regions between the two groups, 498 were more robust in FFC-fed mice compared with Chow-fed mice, suggesting a genome-wide active epigenetic regulation in LSEC during NASH development. Furthermore, in combination with RNA-seq, we demonstrated a robust transcriptional upregulation of the adhesion molecule VCAM-1 in LSEC in NASH pathogenesis.

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Project description:Background and Aims: Nonalcoholic steatohepatitis (NASH) will soon become the leading cause of liver transplantation in the US and is also associated with increased COVID-19 mortality. Currently, there are no FDA approved drugs available that slow NASH progression or address NASH liver involvement in COVID-19. Since animal models cannot fully recapitulate human NASH, we hypothesized that stem cells isolated directly from end-stage NASH patient liver may address current knowledge gaps in human NASH pathology. Approach and Results: We devised methods allowing derivation, proliferation, hepatic differentiation and extensive characterization of bipotent ductal organoids from irreversibly damaged NASH patient liver. The transcriptomes of organoids derived from NASH liver, but not healthy liver show significant upregulation of pro-inflammatory and cytochrome p450-related pathways, as well as of known liver fibrosis and tumor markers, with the degree of upregulation being NASH patient-specific.

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Project description:Nonalcoholic steatohepatitis (NASH) is a major cause of liver fibrosis with increasing prevalence worldwide. Currently there are no approved drugs available. The development of new therapies is difficult as diagnosis and staging requires biopsies. Consequently, predictive plasma biomarkers would be useful for drug development. To identify new plasma biomarkers in a choline-deficient L-amino acid-defined diet rat NASH model we analyzed liver and plasma samples by proteomics, revealing disease relevant signatures and a high correlation between liver mRNA and protein changes. We developed a multi-dimensional attribute ranking approach integrating multi-omics data with liver histology and prior knowledge uncovering known human markers, but also novel candidates. Using regression analysis, we show that the top-ranked plasma markers were highly predictive for fibrosis in our model and hence can serve as preclinical plasma biomarkers. Our approach presented here illustrates the power of multi-omics analyses combined with plasma proteomics and is readily applicable to human biomarker discovery.

2020-01-28 | PXD014751 | Pride

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2023-04-28 | MSV000091820 | MassIVE

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