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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq identifies novel transcript elements and transcript processing in the normal and failing hearts

ABSTRACT: Changes in gene expression contribute to the pathogenesis of heart failure. The sequence, expression level, and structure of the human cardiac transcriptome are incompletely described, as are their changes in heart disease. High throughput transcriptome sequencing (RNA-seq) is a quantitative and unbiased approach to measure transcript level and to identify novel transcribed elements or transcript splicing. Here we acquired 975.2 x 106 mapped RNA-seq reads in 15 control and 15 ischemic cardiomyopathy (ICM) hearts, obtained at the time of heart transplantation. We identified over 1000 differentially expressed transcripts, and thousands of novel transcribed elements, some of which were differentially expressed in between control and ICM groups. We found that transcript processing of several cardiac genes was deranged in ICM. For instance, the ratio between specific MYH6 exons was significantly changed in ICM compared to controls, while this type of inter-exon variation was not observed for the adjoining gene MYH7. This RNA-seq study of the human heart failure transcriptome revealed the diversity of transcripts expressed in the human heart and their complex patterns of expression in the diseased heart. Transcriptome profiling (RNA-seq) of 15 control and 15 ischemic cardiomyopathy (ICM) hearts using Illumina GAII and SOLiD

ORGANISM(S): Homo sapiens

SUBMITTER: LIGUO WANG

PROVIDER: E-GEOD-48166 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RNA-seq identifies novel transcript elements and transcript processing in the normal and failing hearts

Project description:Changes in gene expression contribute to the pathogenesis of heart failure. The sequence, expression level, and structure of the human cardiac transcriptome are incompletely described, as are their changes in heart disease. High throughput transcriptome sequencing (RNA-seq) is a quantitative and unbiased approach to measure transcript level and to identify novel transcribed elements or transcript splicing. Here we acquired 975.2 x 106 mapped RNA-seq reads in 15 control and 15 ischemic cardiomyopathy (ICM) hearts, obtained at the time of heart transplantation. We identified over 1000 differentially expressed transcripts, and thousands of novel transcribed elements, some of which were differentially expressed in between control and ICM groups. We found that transcript processing of several cardiac genes was deranged in ICM. For instance, the ratio between specific MYH6 exons was significantly changed in ICM compared to controls, while this type of inter-exon variation was not observed for the adjoining gene MYH7. This RNA-seq study of the human heart failure transcriptome revealed the diversity of transcripts expressed in the human heart and their complex patterns of expression in the diseased heart.

2013-12-19 | GSE48166 | GEO

Expression data from human heart

Project description:Global gene expression is altered in heart failure. This syndrome can be caused by cardiovascular diseases, including dilated cardiomyopathy (DCM), ischemic cardiomyopathy (ICM), hypertrophic cardiomyopathy, viral or toxic myocarditis, hypertension, and valvular diseases. We used microarrays to evaluate the impact of heart failure on human nucleocytoplasmic transport-related genes examining simultaneoulsly both dilated and ischemic human cardiomyopathies compared to normal hearts.

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Transcription profiling of human heart with heart failure due to ischemic cardiomyopathy or dilated cardiomyopathy

Project description:End stage heart failure due to ischemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM) have similar characteristics, enlargement of the ventricles, relatively thin-walled ventricle, which leads to a limited contraction force and blood loading. Nevertheless, the response for present therapeutics is very variable and the prognosis is still very bad for ICM and DCM in general. Thus, the ability to differentiate the etiologies of heart failure based structural and physiological changes of the heart would be a step forward to enhance the specificity and the success of given therapy.

2007-10-31 | E-CVDE-1 | biostudies-arrayexpress

Transcription profiling of human non ischemic cardiomyopathy (NICM)- (n=12) NYHA III-IV CHF patients

Project description:Inflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control. Experiment Overall Design: Gene expression profiling was performed in three patients' groups: 1) Ischemic cardiomyopathy (ICM)- (n=12) and 2) Non ischemic cardiomyopathy (NICM)- (n=12) NYHA III-IV CHF patients ; 3) Age- and gender matched controls (n=12) by Affymetrix microarrays. Data were then subjected to informatic analysis.

2008-06-17 | E-GEOD-9128 | biostudies-arrayexpress

Isoform-specific regulation of NCAM1 gene expression in ischemic cardiomyopathy

Project description:Although ischemic cardiomyopathy (ICM) is the leading cause of chronic heart failure, one of the most common diseases overall, many aspects of the molecular pathogenesis of ICM still remain to be clarified. It has been We have previously shown that the neural cell adhesion molecule (NCAM1, CD56) is upregulated in ischemic cardiomyopathy by novel isoforms of the transcription factor RUNX1 (AML1) and, in the current study, we show that this upregulation is attributed exclusively to the NCAM1 isoform CD56-140kD. Moreover, we show that the upregulation of CD56-140kD has proapoptotic and antiproliferative effects on cardiomyocytes in vitro as well as inducing mitochondrial damage and reducing the capacity for Ca2+-uptake. As loss of cells and negative inotropy have previously been identified as major components in the development of ischemic cardiomyopathy, these data suggest that the upregulation of CD56-140kD may play a relevant role in the pathogenesis of ICM and therapeutic strategies targeting this molecule may prove to be valuable tools in the management of this very common and often fatal disease in the future.

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Mass spectrometry-based redox and protein profiling reveals distinct protein expression and oxidation patterns in failing human hearts

Project description:Oxidative stress plays a key role in development and progression of cardiovascular diseases and it is correlated with left ventricular dysfunction and heart failure (HF). Oxidative environments lead to the formation of intra- and intermolecular disulfide bonds, as well as to plethora of other reversible and irreversible oxidative amino acid modifications, affecting the functionality of the proteins. Here we report that heart failure due to ischemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) is correlated with increase in oxidative stress compared to non-failing control hearts, manifested through decreased GSH/GSSG ratio in failing heart tissue samples and adaptations of cardiac redox proteome which occur in correlation with two different heart pathologies.

2021-09-09 | PXD021261 | Pride

Distinct Circulating Expression Profiles of Long Non-coding RNAs in Heart Failure Patients with Ischemic and Non- ischemic Dilated Cardiomyopathy

Project description:Ischemic cardiomyopathy(ICM) and dilated cardiomyopathy(DCM), with distinct long-term prognosis and responses to treatment, are two major problems that lead to heart failure(HF) ultimately. In this study, we investigated the lncRNA and mRNA expressions in the plasma of patients with DCM and ICM and analyzed the different lncRNA profile between the two groups. These findings revealed for the first time the specific expression pattern of both protein-coding RNAs and lncRNAs in plasma of HF patients due to DCM and ICM which may provide some important evidence to conveniently identify the etiology of myocardial dysfunctions and help to explore a better strategy for future HF prognosis evaluation.

2022-10-08 | GSE138678 | GEO

Sarcomeric Proteoform Landscape in Ischemic Cardiomyopathy Defined by Top-down Proteomics

Project description:In ischemic cardiomyopathy (ICM), left ventricular systolic dysfunction leads to reduced blood flow and oxygen supply to the heart. Alterations in sarcomeric protein function and expression play prominent roles in the onset and progression of cardiomyopathies; however, the molecular mechanisms underlying ICM remain poorly defined. Herein, we have implemented a top-down liquid chromatography (LC)-mass spectrometry (MS)-based proteomics method for the simultaneous quantification of sarcomeric protein expression and modifications in non-failing donor (n = 16) compared to end-stage failing ICM (n = 16) human cardiac tissues. Our top-down proteomics platform provided a “bird’s eye view” of proteoform families with high mass accuracy and reproducibility. In addition, quantification of post-translational modifications (PTMs) and expression reveal significant changes in various sarcomeric proteins extracted from ICM tissues. Changes include altered phosphorylation and expression of cardiac troponin I (cTnI) and enigma homolog 2 (ENH2) as well as a marked increase in muscle LIM protein (MLP) and calsarcin-1 phosphorylation in ICM hearts. Our results imply that the contractile apparatus of the sarcomere is severely dysregulated during ICM. Thus, this study is the first to uncover significant molecular changes to multiple sarcomeric proteins in end-stage ischemic heart failure patients using LC-MS-based top-down proteomics.

2023-02-20 | PXD038066 | Pride

RNA-seq analysis of human heart failure

Project description:The goal of this study is to compare the transcriptome of heart failure patients (with ischemic or dilated cardiomyopathy) undergoing heart transplantation compared with healthy controls. We analyzed 36 human samples. 13 from ischemic and 13 from dilated human hearts compared with 10 healthy control donors.

2014-04-28 | E-GEOD-55296 | biostudies-arrayexpress

Characterization of proteomic changes in human heart failure

Project description:The microtubule (MT) cytoskeleton can provide a mechanical resistance that can impede the motion of contracting cardiomyocytes. Yet a role of the MT network in human heart failure is unexplored. Here we utilize mass spectrometry to characterize changes to the cytoskeleton in human heart failure. Proteomic analysis of left ventricle tissue reveals a consistent upregulation and stabilization of intermediate filaments and MTs in human heart failure. This dataset includes left ventricular (LV) myocardium from 34 human hearts – either non-failing (NF) or failing hearts. NF hearts are subdivided into normal or compensated hypertrophy (cHyp), while failing hearts are subdivided into ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), and hypertrophic cardiomyopathy with preserved or reduced ejection fraction (HCMpEF and HCMrEF, respectively). Further details on patient classification and in vivo parameters on each heart are listed in sample details.txt.

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