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PRDX1 Cys52Ser Variant Alleviates Nonalcoholic Steatohepatitis by Reducing Inflammation in Mice

ABSTRACT: PRDX1 Cys52Ser Variant Alleviates Nonalcoholic Steatohepatitis by Reducing Inflammation in Mice

PROVIDER: PRJNA1002793 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25541709_1.fastq.gz	Fastqsanger.gz
	SRR25541709_2.fastq.gz	Fastqsanger.gz
	SRR25541710_1.fastq.gz	Fastqsanger.gz
	SRR25541710_2.fastq.gz	Fastqsanger.gz
	SRR25541711_1.fastq.gz	Fastqsanger.gz

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PRDX1 Cys52Ser Variant Alleviates Nonalcoholic Steatohepatitis by Reducing Inflammation in Mice

Project description:Objective: Peroxiredoxin 1 (PRDX1) is a peroxidase and guards against oxidative stress by scavenging intracellular peroxides, whereas it also has been shown to stimulate inflammatory response by functioning as a chaperone protein. The potential in vivo link between PRDX1’s peroxidase activity and its pro-inflammatory activity remains elusive. Methods: We generated peroxidase-dead PRDX1 variant mice by mutating its peroxidatic cysteine at 52 (Cys52) to serine, here referred to as PRDX1Cys52Ser. Trx-TrxR-NADPH coupled activity assay was applied to evaluate the peroxidase activity of global PRDX in PRDX1Cys52Ser variant mice. PRDX1Cys52Ser mice and their wild-type littermates were subjected to western diet or methionine and choline deficient diet feeding. NASH phenotypes were assessed through different analyses including physiological measurements, immunohistochemical staining, and quantitative PCR (qPCR). RNA sequencing, qPCR and western blotting were used to reveal and validate any changes in the signaling pathways responsible for the altered NASH phenotypes observed between WT and PRDX1Cys52Ser variant mice. Results: PRDX1Cys52Ser variant mice showed impaired global PRDX peroxidase activity and reduced susceptibility to diet-induced NASH and liver fibrosis. Mechanistically, PRDX1 Cys52Ser variant suppressed NF-κB signaling and STAT1 signaling pathways that are known to promote inflammation and NASH. Conclusion: The peroxidatic Cys52 of PRDX1 is required for its pro-inflammatory activity in vivo. This study further suggests that PRDX1 plays dual but opposing roles in NASH

2023-08-11 | GSE240198 | GEO

Nonalcoholic steatohepatitis in adolescents undergoing bariatric surgery

Project description:The genomic landscape of hepatic tissue affected by nonalcoholic steatohepatitis (NASH) in severely obese adolescents undergoing bariatric surgery is unknown. Our purpose here was to uncover genomic profiles of obese controls, and obese cases with nonalcoholic fatty liver disease (NAFLD), borderline nonalcoholic steatohepatitis, and definite nonalcoholic steatohepatitis, in order to clarify molecular functions, biological processes, and pathways that are dysregulated in nonalcoholic steatohepatitis in the severely obese adolescent. In a prospective observational cohort study, we have intra-operatively obtained 165 liver samples; of these 67 were submited for microarray analysis. Through ANOVA, we found 8648 genes with differential regulation between the four histologies; from these, we uncovered gene signatures shared between borderline and definite nonalcoholic steatohepatitis, and gene sets with differential effects between borderline and definite.

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Myeloid FoxO1 in Nonalcoholic Steatohepatitis

Project description:Myeloid FoxO1 in Nonalcoholic Steatohepatitis

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AGXT overexpression during nonalcoholic steatohepatitis in mice

Project description:To investigate the effects of AAV8-mediated overexpression of AGXT in mice with diet-induced nonalcoholic steatohepatitis compared to AAV8-GFP

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Nonalcoholic fatty liver, but not nonalcoholic steatohepatitis is a protective factor to tetrachloroethylene-associated kidney effects in male C57BL/6J mice

Project description:Purpose: We investigated the tetrachloroethylene associated changes in kidney transcriptomes among healthy mice, nonalcoholic fatty liver disease mice, and nonalcoholic steatohepatitis mice.

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AGXT overexpression during nonalcoholic steatohepatitis in mice

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Hepatic microRNA signatures in experimental nonalcoholic steatohepatitis

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SOX9 ameliorates nonalcoholic steatohepatitis through activating AMPK pathway

Project description:SOX9 ameliorates nonalcoholic steatohepatitis through activating AMPK pathway

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Liver lipophagy ameliorates nonalcoholic steatohepatitis through lysosomal lipid exocytosis

Project description:Nonalcoholic steatohepatitis (NASH) is a progressive disorder with aberrant lipid accumulation and subsequent inflammatory and profibrotic response. Lipid reduction through cytoplasmic lipolysis might adversely worsen steatohepatitis, however, the effect of autophagic lipolysis, lipophagy, remains obscure. We engineered the adaptor protein to induce lipophagy with lipid droplet targeting signal and modified LC3 interacting region. Activating hepatocyte lipophagy obviously mitigated both steatosis and NASH pathology. Mechanistically, lipophagy promoted the excretion of lipid from liver via lysosomal exocytosis and attenuated harmful accumulation of nonesterified fatty acid. This exocytosis was dependent on Ca2+ signal unlike the lysosomal dysfunction-related exocytosis. High content compound screening identified alpelisib and digoxin, clinically-approved compounds, as effective activators of lipophagy. Administration of alpelisib or digoxin inhibited the transition to steatohepatitis in mice fed high fat with low methionine low choline diet. Given all these data, activating lipophagy may be a promising therapeutic approach to prevent NASH progression.

2023-05-15 | GSE185911 | GEO

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