Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: diego arcelli

PROVIDER: E-GEOD-9128 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

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.

2014-12-01 | GSE34124 | GEO

Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy: left ventricle DCM

Project description:We wanted to see whether the set of affected genes in ischemic cardiomyopathy (ICM) is the same or different as compared to dilated cardiomyopathy (DCM). To find this out, we placed the single DCM sample on the same microarray slide with the ICM samples. Analysis of microarray data with ICM samples only showed 63 affected genes, while that carried out with 2 ICM samples PLUS one DCM sample reduced this number to just four genes. From this result we conclude that ICM and DCM affect different sets of genes in ventricular myocytes. Keywords: Expression profiling by array From the associated publication: To find out whether the splice microarray results reported in Table 3 are disease-type specific, we supplemented the same splice microarray of ICM ventricular myocytes with one additional sample prepared from left ventricle of a 41-years old dilated cardiomyopathy male donor. The top-list ANOVA gene score annotation for combined altered CE&P genes in ventricular myocytes (Table 3) was reduced from 63 to just 4 genes (FXYD1 (Gfold = +2.4), HCN2 (-1.5), GLRA1 (-1.8) and GJC1 (-2.3)).

2010-06-17 | E-GEOD-17530 | biostudies-arrayexpress

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

Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy: left ventricle DCM

2010-06-17 | GSE17530 | GEO

Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy

2010-02-18 | GSE17294 | 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

Molecular Remodeling of Ion Channels in Human Atrial and Ventricular Myocytes Associated with Ischemic Cardiomyopathy

Project description:Ischemic cardiomyopathy (ICM) leads to congestive heart failure and can cause sudden cardiac death due to arrhythmia. Existing molecular knowledge base of ICM is rudimentary because of lack of specific attribution to cell type and function. This study was designed to investigate cell-specific molecular remodeling of ion channels, exchangers and pumps, which are signaling molecules (SM) involved in electrical, signaling and mechanical functions of the heart. Atrial and ventricular myocytes were isolated by laser-capture microdissection from left atrium and ventricle of healthy and ICM human hearts. SM and their splice variants altered by ICM in cardiomyocytes were identified by splice microarray and validated by RT-PCR. Molecular profiling of ICM-related changes showed that SM in atrial and ventricular myocytes remodel following their unique programs. ICM affected 63 genes in ventricular myocytes and 12 genes in atrial myocytes. Only few of the identified genes were previously linked to human cardiac disfunctions. In our experiments we used 3 healthy hearts rejected from transplantation procedure and explanted ICM hearts from three male patients. Tissue samples were dissected from left ventricle and left atrial appendages. Atrial and ventricular myocytes were laser-capture microdissected from serial 7-8-Âµm thick cryostat sections. Individual cellular total RNA samples were analyzed on custom-built Human Ion Channel Splice Arrays slides (ExonHit) manufactured on the Ion Channel Splice Array sv1.1 platform representing 287 human SM, including 248 alternatively spliced ones in total 1655 splicing events and supplemented with capabilities to recognize connexins and ryanodine receptors.

2010-05-14 | E-GEOD-17294 | biostudies-arrayexpress

Proteomic analysis of ischemic and dilated cardiomyopathy pre-mortem human hearts

Project description:Our understanding of heart failure (HF) has been provided by indirect surrogates, such as post-mortem histology, cardiovascular imaging, and molecular characterisation in vivo and in vitro, rather than directly in pre-mortem human cardiac tissue. Using our heart bank of pre-mortem hearts procured according to the most stringent protocols, we examined ischemic (ICM) and dilated cardiomyopathy (DCM) -- the most common causes of HF and leading causes of cardiac transplantation1. We performed unbiased, comprehensive, paired proteomic and metabolomic analysis of 51 left ventricular (LV) samples from 44 cryopreserved pre-mortem human ICM and DCM hearts, including age-matched, healthy, histopathologically-normal donor controls of both genders for comparison. Data integration via pathway and correlation network analysis revealed overlapping and divergent disease pathways in ICM and DCM, and, strikingly, precise sex-specific differences within each disease that unveil the interaction of gender with HF. Identified core functional nodes in each disease may serve as novel therapeutic targets, and we provide all proteomic and metabolomic results via an interactive online repository (https://mengboli.shinyapps.io/heartomics/) as a publicly available resource.

2020-05-01 | PXD018678 | Pride

Transcription profiling of human hearts exhibiting ischemic and nonischemic cardiomyopathy

Project description:Pre-LVAD and explanted ischemic and nonischemic cardiomyopathy and nonfailing hearts all normalized with RMA

2007-08-25 | E-GEOD-1869 | biostudies-arrayexpress