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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

PRDX1 Cys52Ser variant alleviates nonalcoholic steatohepatitis by reducing inflammation in mice.

Project description:ObjectivePeroxiredoxin 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.MethodsWe 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.ResultsPRDX1Cys52Ser 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.ConclusionThe peroxidatic Cys52 of PRDX1 is required for its pro-inflammatory activity in vivo. This study further suggests that PRDX1 may play dual but opposing roles in NASH.

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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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Project description:Nonalcoholic steatohepatitis (NASH) is an advanced form of nonalcoholic fatty liver disease with adverse outcomes that currently lacks approved medication. Muscle-liver interaction has emerged as one of the critical determinants governing NASH progression. Here, we report that remote limb ischemic conditioning (RIC), a clinically validated therapy for distant ischemic organ protection by transient muscle ischemia, significantly alleviated NASH in different mouse models. The anti-NASH effect of chronic RIC treatment was mediated by the muscle-to-liver transfer of extracellular vesicles (EVs) and their cargo microRNAs, leading to elevation of miR-181d-5p in the liver. Hepatic miR-181d-5p overexpression faithfully mirrored the benefits of RIC treatment via suppression of nuclear receptor 4A3. Furthermore, administration of circulating EVs from human volunteers undergoing RIC treatment improved NASH phenotypes and transcriptomic perturbations in primary human hepatocytes and animal models. Our data underscore the translational potential of RIC treatment for NASH management and extend our understanding of muscle-liver crosstalk.

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Remote limb ischemic conditioning alleviates nonalcoholic steatohepatitis via extracellular vesicle-mediated muscle-liver crosstalk [hEV_RNAseq]

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Project description:Neutralization of Oxidized Phospholipids Restrains Nonalcoholic Steatohepatitis

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