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Human Cardiac Proteome of Hypertrophic Cardiomyopathy

ABSTRACT: This study utilized TMT to characterize the cardiac proteomic differences between patients with hypertrophic cardiomyopathy and controls.

INSTRUMENT(S): QExactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Dr. Michael Ackerman

PROVIDER: MSV000091821 | MassIVE | Fri Apr 28 22:21:00 BST 2023

REPOSITORIES: MassIVE

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Publications

Multi-Omic Architecture of Obstructive Hypertrophic Cardiomyopathy.

Garmany Ramin R Bos J Martijn JM Tester David J DJ Giudicessi John R JR Dos Remedios Cristobal G CG Dasari Surendra S Nagaraj Nagaswaroop K NK Nair Asha A AA Johnson Kenneth L KL Ryan Zachary C ZC Maleszewski Joseph J JJ Ommen Steve R SR Dearani Joseph A JA Ackerman Michael J MJ

Circulation. Genomic and precision medicine 20230220 2

<h4>Background</h4>Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric left ventricular hypertrophy. Currently, hypertrophy pathways responsible for HCM have not been fully elucidated. Their identification could serve as a nidus for the generation of novel therapeutics aimed at halting disease development or progression. Herein, we performed a comprehensive multi-omic characterization of hypertrophy pathways in HCM.<h4>Methods</h4>Flash-frozen cardiac tissues were collected from gen ...[more]

PMID: 36802768

Publication: 1/2

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Human hypertrophic cardiomyopathy cardiac tissue phosphoproteomics

Project description:This study used TMT-pro method to look for phosphoproteomic differences in heart tissue of patients with hypertrophic cardiomyopathy and controls

2023-04-28 | MSV000091822 | MassIVE

Human Hypertrophic Cardiomyopathy mRNA Profiling.

Project description:Cardiac biopsies were obtained from hypertrophic cardiomyopathy (HCM) patients and controls and subjected to mRNA profiling.

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Alteration in Tyrosine Phosphorylation of Cardiac Proteome and EGFR Pathway Contribute to Hypertrophic Cardiomyopathy

Project description:Alterations of serine/threonine phosphorylation of the cardiac proteome are a hallmark of heart failure. However, the contribution of tyrosine phosphorylation (pTyr) to the pathogenesis of cardiac hypertrophy remains unclear. We use global mapping to discover and quantify site-specific pTyr in two cardiac hypertrophic mouse models, i.e., cardiac overexpression of ErbB2 (TgErbB2) and myosin heavy chain R403Q (R403Q-aMyHC Tg), compared to control hearts. From this, there are significant phosphoproteomic alterations in TgErbB2 mice in right ventricular cardiomyopathy, hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM) pathways. On the other hand, R403Q-aMyHC Tg mice indicated that the EGFR1 pathway is central for cardiac hypertrophy, along with angiopoietin, ErbB, growth hormone, and chemokine signaling pathways activation. Surprisingly, most myofilament proteins have downregulation of pTyr rather than upregulation. Kinase-substrate enrichment analysis (KSEA) shows a marked downregulation of MAPK pathway activity downstream of k-Ras in TgErbB2 mice and activation of EGFR, focal adhesion, PDGFR, and actin cytoskeleton pathways. In vivo ErbB2 inhibition by AG-825 decreases cardiomyocyte disarray. Serine/threonine and tyrosine phosphoproteome confirms the above-described pathways and the effectiveness of AG-825 treatment. Thus, altered pTyr may play a regulatory role in cardiac hypertrophic models.

2023-03-10 | PXD036506 | Pride

MicroRNA Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

Project description:Using a high-throughput gene expression profiling technology, we have illuminated novel potential microRNA (miRNA) components of the molecular disease process underlying human hypertrophic cardiomyopathy (HCM). It is hoped that this will fuel future research endeavors that will eventually uncover the role miRNAs may play in the phenotypic heterogeneity of the disease, and thus, provide potential tools for identifying patients with benign versus malignant forms of the disease. Case (n = 107)-Control (n=20) study comparing the microRNA transcriptome of cardiac tissues from patients with hypertrophic cardiomyopathy to the microRNA transcriptome of control donor cardiac tissues.

2012-09-01 | E-GEOD-36946 | biostudies-arrayexpress

Transcriptome Profiling of Surgical Myectomy Tissue from Patients with Hypertrophic Cardiomyopathy

Project description:Using a high-throughput gene expression profiling technology, we have been able to develop new hypotheses regarding the molecular pathogenic mechanisms of human hypertrophic cardiomyopathy (HCM). It is hoped that these hypotheses, among others generated by this data, will fuel future research endeavors that will uncover novel biomarkers, prognostic indicators, and therapeutic targets to improve our ability to diagnose, counsel, and treat patients with this highly heterogeneous and potentially life-threatening condition. Case-control study comparing the messenger RNA transcriptome of cardiac tissues from patients with hypertrophic cardiomyopathy to the transcriptome of control donor cardiac tissues.

2012-09-01 | E-GEOD-36961 | biostudies-arrayexpress

Altered Cardiac Energetics and Mitochondrial Dysfunction in Hypertrophic Cardiomyopathy

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Cardiac Proteomic Profiling in Hypertrophic and Dilated Cardiomyopathy

Project description:Hypertrophic cardiomyopathy and dilated cardiomyopathy are different diseases with distinct clinical manifestations, and the confounding pathogenic mechanisms behind them remains unclear. The purpose of this study was to find out the crucial proteins and pathways in severe cardiomyopathy patients, through the proteomic technology in myocardial tissues.

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Microarray Analysis of a Familial Hypertrophic Cardiomyopathy Mouse Model Rescued by a Phospholamban Knockout

Project description:Familial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function. Our laboratories have previously developed 2 mouse models that affect cardiac performance. One transgenic mouse model encodes an FHC-associated mutation in α-tropomyosin (Tm180) that displays severe cardiac hypertrophy with fibrosis and impaired physiological performance. The other model was a gene knockout of phospholamban (PLB), a regulator of calcium uptake in the sarcoplasmic reticulum of cardiomyocytes; the hearts of these mice exhibit hypercontractility with no pathological abnormalities. Previous work in our laboratories show that the hearts of mice that were genetically crossed between the Tm180 and PLB KO mice rescues the hypertrophic phenotype and improves their cardiac morphology and function. We used microarrays to detail the global program of gene expression underlying cardiac remodeling and rescue of the hypertrophic cardiomyopathic phenotype and identified distinct classes of regulated genes during this process. To understand the changes in gene expression that occur over time in these animal models (Tm180, PLB KO, Tm180/PLB KO and nontransgenic control mice), we conducted microarray analyses of left ventricular tissue at 4 and 12 months of age.

2012-12-13 | E-GEOD-42892 | biostudies-arrayexpress

Human Hypertrophic Cardiomyopathy mRNA Profiling.

Project description:Human Hypertrophic Cardiomyopathy mRNA Profiling.

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Sexual Dimorphism in Cardiac Transcriptome Associated with a Troponin C Murine Model of Hypertrophic Cardiomyopathy

Project description:Heart disease remains the number one killer of women in the US. Nonetheless, studies in women and female animal models continue to be underrepresented in cardiac research. Hypertrophic cardiomyopathy (HCM), the most commonly inherited cardiac disorder, has been tied to sarcomeric protein variants. Among the susceptible genes, TNNC1—encoding cardiac troponin C (cTnC)—has contributed to a substantial HCM phenotype in mice. In this study we sought to characterize the sexual dimorphism observed within cardiac physiology and transcriptomics of adult male and female mice bearing the HCM-associated cTnC-A8V point mutation. The HCM mice showed a significant decrease in stroke volume, left ventricular diameter, volume, and relative wall thickness. Importantly, isovolumetric contraction time was significantly higher for female HCM mice. RNA sequencing revealed several altered canonical pathways within the HCM mice vs WT groups including an increase in EIF2 signaling, ILK signaling, actin nucleation by ARP-WASP complex, regulation of actin-based motility by Rho, VDR/RXR activation, and glutathione redox reactions pathways. In contrast, Valine Degradation, TCA Cycle II, Methionine Degradation, and Inositol Phosphate Compound pathways were notably down regulated in HCM mice. HCM male vs. female mice followed similar trends of the canonical pathways altered between the HCM and WT. Interestingly, seven of the genes that were differentially expressed in both the WT and HCM male vs female comparisons changed directions in fold change between the sexes. These data suggest a sexually-dimorphic HCM phenotype and identify several key pathways and genes that could be critical to sex differences seen in disease manifestation.

2020-01-23 | GSE144098 | GEO

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