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PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

ABSTRACT: PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

PROVIDER: PRJNA1102894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28759733.fastq.gz	Fastqsanger.gz
	SRR28759734.fastq.gz	Fastqsanger.gz
	SRR28759735.fastq.gz	Fastqsanger.gz
	SRR28759736.fastq.gz	Fastqsanger.gz
	SRR28759737.fastq.gz	Fastqsanger.gz

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PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Western Diet + CCl4]

Project description:Somatic mutations in non-malignant tissues are selected for because they confer increased clonal fitness, however, it is uncertain if these clones can benefit organ health. Here, ultra-deep targeted sequencing of 150 liver samples from 30 chronic liver disease patients revealed recurrent somatic mutations. PKD1 mutations were observed in 30% of patients, whereas they were only detected in 1.3% of hepatocellular carcinomas (HCCs). To interrogate tumor suppressor functionality, we perturbed PKD1 in two HCC cell lines and six in vivo models, in some cases showing that PKD1 loss protected against HCC, but in most cases showing no impact. However, Pkd1 haploinsufficiency accelerated regeneration after partial hepatectomy. We tested Pkd1 in fatty liver disease, showing that Pkd1 loss was protective against steatosis and glucose intolerance. Mechanistically, Pkd1 loss selectively increased mTOR signaling without SREBP activation. In summary, PKD1 mutations in cirrhotic livers exert adaptive functionality without increasing transformation risk.

2024-05-15 | GSE264521 | GEO

PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

2024-05-15 | GSE264520 | GEO

PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

Project description:PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer [Normal Chow diet]

| PRJNA1102893 | ENA

Gene expression profiling unravels cancer-related hepatic molecular signatures in steatohepatitis but not in steatosis

Project description:Pathogenesis and factors for determining progression of alcoholic and non-alcoholic steatosis to steatohepatitis with risk of further progression to liver cirrhosis and cancer are poorly understood. In the present study, we aimed to identify potential molecular signatures for discrimination of steatohepatitis from steatosis. Global gene expression analysis was applied to unravel differentially expressed genes between steatohepatitis compared to steatosis and control samples. For functional annotation as well as the identification of disease-relevant biological processes of the differentially expressed genes the gene ontology (GO) database was used. Genes down-regulated in steatohepatitis were mainly involved in metabolic processes. Genes up-regulated in steatohepatitis samples were associated with cancer progression and proliferation. Further statistical and pathway analysis lead to the selection of 46 candidate genes which were validated in two sample cohorts by quantitative real-time PCR. In surgical liver resection samples 39 genes and in percutaneous liver biopsies 30 genes were significantly up-regulated in steatohepatitis. Conclusion: The development of steatohepatitis is characterized by distinct molecular changes. 44 human liver tissue surgical samples (normal n=13; steatosis n=19; steatohepatitis n=12, 8/2 cirrhotic/non-cirrhotic) obtained from patients undergoing liver surgery for HCC, other malignancy/metastatic disease, benign tumors of the liver and organ dedicated to transplantation. Virtually normal control samples in this cohort were taken from patients undergoing surgical resection of liver metastasis, but the surrounding liver tissue used for the molecular analyses was normal, non-tumorous liver tissue without detectable pathological changes. The samples were provided by the Biobank at the Medical University of Graz. This dataset is part of the TransQST collection.

2012-12-10 | E-GEOD-33814 | biostudies-arrayexpress

PKD1

Project description:PKD1 gene and protein study

| PRJEB28230 | ENA

Project description:PKD1 mutant clones within cirrhotic livers inhibit steatohepatitis without promoting cancer

| PRJNA1102869 | ENA

Pkd1 and Pkd2 mRNA cis-inhibition drives polycystic kidney disease progression [Pkd1]

Project description:We report the findings of deletion of the miR17 binding motif from Pkd1 mRNA

2022-02-11 | GSE196588 | GEO

Effect of CVX-060 treatment on hepatic gene expression of cirrhotic rats

Project description:Currently, the therapeutic prospects for cirrhosis patients are limited to liver transplantation and, therefore, there is an urgent need to develop new therapeutic strategies for improved treatments. Cirrhosis was induced in male Wistar rats with CCl4 treatment, and RNA from the complete livers was extracted and quantified through microarray experiments. Angiopoietins signalling is a key pathway in blood vessel normalization. Angiopoietin 1 (Ang1)-Tie2 signalling stabilizes blood vessels, Angiopoietin 2 (Ang2) on the other hand is a context-dependent antagonist of Ang1 and decreases its stabilizing effect giving rise to immature blood vessels. Cirrhotic conditions are characterized by higher expression and activity of Ang2 than healthy conditions, resulting in the loss of blood vessels stability. Previous work showed that inhibition of Ang2 via CVX-060 enhances Ang1-Tie2 signalling, and can stabilize the vascular system in cirrhotic livers. We therefore performed RNA extraction after treatment of cirrhotic rats with CVX-060 during 4 weeks. We observed changes in expression state (expressed/not expressed) in key transcription factors previously implicated in cirrhosis.

2019-03-22 | GSE122822 | GEO

The synergestic effects of western diet and carbon tetrachloride (CCl4) to develop non-alcoholic steatohepatitis (NASH) and liver tumor in mice

Project description:NASH is a combination of hepatic steatosis and severe inflammation, which can lead to fatal liver disease such as cirrhosis and hepatocellular carcinoma. While a variety of models have been descirbed, they have several limitations. Therefore, it is of urgent importance to create animal model that recapitulate the physiology, histology and outcome seen in human with NASH. We created western diet-fed and CCl4-treated mouse model. they showed characteristic histological features of NASH such as fibrosis, ballooning and steatosis at 12 weeks and liver cancers developed at 24 weeks. Their transcritomic changes were also similar to those seen in human NASH.

2018-03-28 | GSE99010 | GEO

Dehydration facilitates cyst formation and growth in Pkd1-/- mice via macrophage

Project description:The Pkd1 gene was inactivated by tamoxifen at postnatal day 30 (P30) to generate a chronic-onset conditional Pkd1 gene knockout mouse model. Without any intervention, micro cysts could be detected adjacent to renal medulla-corticomedullary junction in Pkd1-/- mice until P180 and cystic phenotype is severe at P300. However, under dehydration situation, the cyst growth was more accelerated and progressive. The dehydration protocol resulted in Pkd1-/- mice varying degrees of sweating and weight loss. Mice that were not provided water during the day (water at night (D-WAN)) and mice that had access to water during the day (water all time (D-WAT)) showed significantly more weight loss compared with the control Pkd1-/- mice, although they drank more water at night. Interestingly, although D-WAN Pkd1-/- mice and D-WAT Pkd1-/- mice lost approximately body weights after one-day dehydration, while cyst enlargement and renal dysfunction was much more severe in the D-WAN Pkd1-/- mice after two-month intervention.

2021-04-27 | E-MTAB-10449 | biostudies-arrayexpress

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