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Transcription profiling of human hearts exhibiting ischemic and nonischemic cardiomyopathy

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

ORGANISM(S): Homo sapiens

DISEASE(S): normal

SUBMITTER: Michelle Kittleson

PROVIDER: E-GEOD-1869 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression analysis of ischemic and nonischemic cardiomyopathy: shared and distinct genes in the development of heart failure.

Kittleson Michelle M MM Minhas Khalid M KM Irizarry Rafael A RA Ye Shui Q SQ Edness Gina G Breton Elayne E Conte John V JV Tomaselli Gordon G Garcia Joe G N JG Hare Joshua M JM

Physiological genomics 20050315 3

Cardiomyopathy can be initiated by many factors, but the pathways from unique inciting mechanisms to the common end point of ventricular dilation and reduced cardiac output are unclear. We previously described a microarray-based prediction algorithm differentiating nonischemic (NICM) from ischemic cardiomyopathy (ICM) using nearest shrunken centroids. Accordingly, we tested the hypothesis that NICM and ICM would have both shared and distinct differentially expressed genes relative to normal hear ...[more]

PMID: 15769906

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Ischemic and Nonischemic CM and NF Hearts

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

2004-10-26 | GSE1869 | GEO

Changes in extracellular matrix in failing human non-ischemic and ischemic hearts with mechanical unloading

Project description:Ischemic and non-ischemic cardiomyopathies have distinct etiologies and underlying disease mechanisms, which require in-depth investigation for improved therapeutic interventions. The goal of this study was to use clinically obtained myocardium from healthy and heart failure patients, and characterize the changes in extracellular matrix (ECM) in ischemic and non-ischemic failing hearts, with and without mechanical unloading. Using tissue engineering methodologies, we also investigated how diseased human ECM, in the absence of systemic factors, can influence cardiomyocyte function. Heart tissues from heart failure patients with ischemic and non-ischemic cardiomyopathy were compared to explore differential disease phenotypes and reverse remodeling potential of left ventricular assisted device (LVAD) support at transcriptomic, proteomic and structural levels. The collected data demonstrated that the differential ECM compositions recapitulated the disease microenvironment and induced cardiomyocytes to undergo disease-like functional alterations. In addition, our study also revealed molecular profiles of non-ischemic and ischemic heart failure patients and explored the underlying mechanisms of etiology-specific impact on clinical outcome of LVAD support and tendency towards reverse remodeling.

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Transcription profiling of human ischemic cardiomyopathy, idiopathic cardiomyopathy, and nonfailing controls

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2008-06-14 | E-GEOD-5406 | 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

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.

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Targeting Immune-Fibroblast Crosstalk in Myocardial Infarction and Cardiac Fibrosis I

Project description:To define the cellular landscape of human myocardial infarction and heart failure, we performed Cellular Indexing of Transcriptomes and Epitomes by sequencing (CITE-seq) in 22 explanted human hearts from healthy donors, acute myocardial infarction (MI),and chronic ischemic and non-ischemic cardiomyopathy patients.

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Human ischemic cardiomyopathy, idiopathic cardiomyopathy, and nonfailing controls

2006-09-04 | GSE5406 | GEO

Transcription profiling of human hearts exhibiting ischemic and nonischemic cardiomyopathy

Project description: Not available

| S-DIXA-D-1049 | biostudies-other

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

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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

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