Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-seq of hepatic biopsies taken from patients with chronic liver disease presenting with different aetiologies (HCV, FLD) and fibrosis stages.

ABSTRACT: To determine gene signatures associated with advanced liver fibrosis, we undertook RNA-sequencing of liver biopsies from patients presenting with different aetiologies (HCV or FLD) and fibrosis stages (n=69 patients). This dataset is part of the TransQST collection.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Divya Ramnath

PROVIDER: E-MTAB-6863 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes.

Ramnath Divya D Irvine Katharine M KM Lukowski Samuel W SW Horsfall Leigh U LU Loh Zhixuan Z Clouston Andrew D AD Patel Preya J PJ Fagan Kevin J KJ Iyer Abishek A Lampe Guy G Stow Jennifer L JL Schroder Kate K Fairlie David P DP Powell Joseph E JE Powell Elizabeth E EE Sweet Matthew J MJ

JCI insight 20180726 14

Chronic liver disease (CLD) is associated with tissue-destructive fibrosis. Considering that common mechanisms drive fibrosis across etiologies, and that steatosis is an important cofactor for pathology, we performed RNA sequencing on liver biopsies of patients with different fibrosis stages, resulting from infection with hepatitis C virus (HCV) (with or without steatosis) or fatty liver disease. In combination with enhanced liver fibrosis score correlation analysis, we reveal a common set of ge ...[more]

PMID: 30046009

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Project description:Advancements in animal models and cell culture techniques have been invaluable in the elucidation of molecular events and mechanisms regulating muscle atrophy. However, few studies have examined muscle atrophy in humans using modern experimental techniques. The purpose of this study was to examine and validate changes in global gene transcription during immobilization-induced muscle atrophy in humans. Healthy men and women (N=24) were subjected to two weeks of unilateral limb immobilization, with muscle biopsies obtained before, and after 48 hours (48H) and 14 days (14D) of immobilization. Both muscle cross sectional area (~ 5 %) and strength (10-20 %) were significantly reduced in men and women after 14D of immobilization. Micro-array analysis of total RNA extracted from biopsy samples uncovered 575 and 3,128 probes representing multiple genes, which were significantly altered at 48H and 14D, respectively. As a group, genes involved in mitochondrial bioenergetics and carbohydrate metabolism were predominant features at both 48H and 14D, with genes involved in protein synthesis and degradation significantly down-regulated and up-regulated, respectively, at 14D of muscle atrophy. There was also a significant decrease in the protein content of mitochondrial cytochrome c oxidase, and the enzyme activity of cytochrome c oxidase and citrate synthase after 14D of immobilization. Furthermore, protein ubiquitination and oxidative damage were significantly increased by 48H and 14D of immobilization, respectively. These results suggest that transcriptional and post-transcriptional suppression of mitochondrial processes is sustained throughout 14D of immobilization, while protein ubiquitination plays an early but transient role in the progression of immobilization-induced muscle atrophy in humans. 72 samples taken from quadriceps of healthy ambulatory young men and women. Samples were taken at 3 timepoints throughout a 14 day period, the initial sample was taken at time 0 (PRECAST), then the limb was immobilized via a brace, and the 2nd sample was taken at 48 hours (CAST02D). The third sample was taken following 14 days of immobilization (CAST14D).

Dataset Information

RNA-seq of hepatic biopsies taken from patients with chronic liver disease presenting with different aetiologies (HCV, FLD) and fibrosis stages.

Publications

Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes.

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