Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of rat 3 months old male Wistar animals by aorto-caval fistula reveals alterations in systemic substrate metabolism in rat volume-overload model of chronic heart failure

ABSTRACT: Abnormalities in metabolism of energetic substrates may play a role in progression of chronic heart failure (HF). The goal of the study was to examine the extent and mechanisms of metabolic alterations in rat model of chronic HF due to volume overload. Volume overload was induced in 3 months old male Wistar rats by aorto-caval fistula. In the phase of symptomatic HF (after 21 weeks), we performed myocardial gene expression analysis. Cardiac tissue gene expression analysis showed downregulation of enzymes of respiratory cycle, mitochondrial fatty acid (FA) oxidation and attenuated expression of proteins responsible for FA translocation/transport (CD36/FAT, FABP3, FATP-1). Simultaneously, we performed gene expression analysis of fat tissue.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Michal Kolar

PROVIDER: E-MTAB-190 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Metabolic characterization of volume overload heart failure due to aorto-caval fistula in rats.

Melenovsky Vojtech V Benes Jan J Skaroupkova Petra P Sedmera David D Strnad Hynek H Kolar Michal M Vlcek Cestmir C Petrak Jiri J Benes Jiri J Papousek Frantisek F Oliyarnyk Olena O Kazdova Ludmila L Cervenka Ludek L

Molecular and cellular biochemistry 20110405 1-2

Metabolic interactions between adipose tissue and the heart may play an active role in progression of heart failure (HF). The aim of the study was to examine changes in myocardial and adipose tissue metabolism and gene expression in a rat HF model induced by chronic volume overload. HF was induced by volume overload from aorto-caval fistula (ACF) in 3-month-old male Wistar rats and animals were studied in the phase of decompensated HF (22nd week). HF rats showed marked eccentric cardiac hypertro ...[more]

PMID: 21465236

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Project description:Normal adult liver is uniquely capable of renewal; and repair after injury. Whether this response; represents simple hyperplasia of various liver elements; or requires recapitulation of the genetic program of; the developing liver is not known. To study these possibilities, we examined transcriptional programs of adult liver after partial hepatectomy and contrasted these with developing embryonic liver. Principal component analysis demonstrated that the time series of gene expression during liver regeneration does not segregate according to developmental transcription patterns. Gene ontology analysis revealed that liver restoration after hepatectomy and liver development differ dramatically with regard to transcription factors and chromatin structure modification. In contrast, the tissues are similar with regard to proliferationassociated genes. Consistent with these findings, realtime polymerase chain reaction showed transcription factors known to be important in liver development are not induced during liver regeneration. These three lines of evidence suggest that at a transcriptional level, restoration of liver mass after injury is best described as hepatocyte hyperplasia and not true regeneration. We speculate this novel pattern of gene expression may underlie the unique capacity of the liver to repair itself after injury. Experiment Overall Design: In order to elucidate the molecular similarities between regenerating and developing liver, we performed high-density microarray analysis using Affymetrix MG 430 2.0 chips for targets at 0, 1, 2, 6, 12, 18, 24, 30, 48, and 72 hours after partial hepatectomy and at 10.5, 11.5, 12.5, 13.5, 14.5, and 16.5 days post conception (dpc). Experiment Overall Design: Each experimental time point is represented by two separate samples, each consisting of at least 3 pooled tissues from different animals. For example, 6 hepatectomies were performed for the 1 hour post-hepatectomy time point. Time 0 is used as control.

Dataset Information

Transcription profiling of rat 3 months old male Wistar animals by aorto-caval fistula reveals alterations in systemic substrate metabolism in rat volume-overload model of chronic heart failure

Publications

Metabolic characterization of volume overload heart failure due to aorto-caval fistula in rats.

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