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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis

ABSTRACT: Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis

PROVIDER: PRJNA534053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8937490_1.fastq.gz	Fastqsanger.gz
	SRR8937490_2.fastq.gz	Fastqsanger.gz
	SRR8937491_1.fastq.gz	Fastqsanger.gz
	SRR8937491_2.fastq.gz	Fastqsanger.gz
	SRR8937482_1.fastq.gz	Fastqsanger.gz

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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis [array]

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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis [RNA-Seq]

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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis [array]

Project description:Our project is to explore the molecular subtypes for targeted therapies in Alcoholic Hepatitis (AH). We have found that LCN2 gene expression is markedly induced in AH patients and correlated to the disease severity including portal hypertension. Animal data from microarray experiments show that compared with the wild mice, LCN2 knockout mice are protected from CCl4-induced liver fibrosis. The focus of our current study is to investigate the effect of overexpression of LCN2 on functional changes in hepatocytes. To this end, HepG2 cells and human primary hepatocytes (HPH) were overexpressed human LCN2 gene and samples were analyzed through RNA-sequencing.

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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis [RNA-Seq]

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Intrahepatic lipocalin 2 promotes liver fibrosis in alcoholic hepatitis

Project description:This SuperSeries is composed of the SubSeries listed below.

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Pathogenesis of alcoholic hepatitis

Project description:Pathogenesis of alcoholic hepatitis

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Transcriptome Analysis Identifies Fn14, a TNF Superfamily Receptor Member, as a Therapeutic Target in Alcoholic Hepatitis

Project description:Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease and occurs in patients with excessive alcohol intake It is characterized by marked hepatocellular damage, steatosis and pericellular fibrosis. Patients with severe AH have a poor short-term prognosis. Unfortunately, current therapies (i.e. corticosteroids and pentoxyphylline) are not effective in many patients and novel targeted therapies are urgently needed. The development of such therapies is hampered by a poor knowledge of the underlying molecular mechanisms. Based on studies from animal models, TNF alfa was proposed to play a pivotal role in the mechanisms of AH. Consequently, drugs interfering TNF alfa were tested in these patients. The results were disappointing due to an increased incidence of severe infections. Unluckily, there are not experimental models that mimic the main findings of AH in humans. To overcome this limitation, translational studies with human samples are required. We previously analyzed samples from patients with biopsy-proven AH. In these previous studies, we identified CXC chemokines as a potential therapeutic target for these patients. We expanded these previous observations by performing a high-throughout transcriptome analysis. Hepatic gene expression profiling was assessed by DNA microarray in patients with Alcoholic hepatitis (n=15) and normal livers (n=7).

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Hepatic cell proliferation and outcome in alcoholic hepatitis: histology, gene expression and effect of stem cell therapy

Project description:Regeneration and alcoholic hepatitis

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Characterization and Function of Neutrophils in Alcoholic Hepatitis in Humans and Mice: Roles for Neutrophilic p47phox in Disease Progression

Project description:Intrahepatic neutrophil infiltration has been implicated in the pathogenesis of severe alcoholic hepatitis (SAH), a disease with high short-term morality; however, how neutrophils contribute to SAH progression remain obscure. This study aimed to characterize intrahepatic neutrophil infiltration and its involvement in AH pathogenesis. We found that hepatic expression of neutrophil cytosolic factor 1 (NCF1), a key factor in controlling neutrophilic ROS production, was upregulated and correlated with neutrophil number, inflammation and ROS-associated genes in SAH patients. Ncf1 floxed mice were generated using CRISPR/Cas9 technology by inserting two LoxP sequences into intron 1 and intron 8 of the mouse Ncf1 gene, then crossed with Lyz Cre mice to generated myeloid cell-specific Ncf1 knockout (Ncf1Lyz-/-) mice. The LyzCre negative Ncf1 floxed mice were used as corresponding WT littermate control. The chronic-plus-binge ethanol feeding model was used in this study. The total RNAs were extracted from ETOH-fed 5 WT and 4 Ncf1Lyz-/- mouse livers and submitted for a Poly(A) RNA sequencing. Genetic deletion of the Ncf1 gene in neutrophils abolished hepatic ROS, inflammation, and fibrosis induced by ethanol feeding. RNA-sequencing analysis and the data from experimental models revealed that neutrophilic NCF1-dependent ROS promoted alcoholic liver injury by inhibiting AMP-activated protein kinase (a key regulator of lipid metabolism) and microRNA-223 (a key anti-inflammatory and anti-fibrotic microRNA). Our data suggest that divergent pathogeneses exist in SAH and neutrophilic NCF1-dependent ROS promotes alcoholic liver injury by inhibiting AMPK and microRNA-223.

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