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

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

PROVIDER: PRJNA602746 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10954100.fastq.gz	Fastqsanger.gz
	SRR10954101.fastq.gz	Fastqsanger.gz
	SRR10954102.fastq.gz	Fastqsanger.gz
	SRR10954103.fastq.gz	Fastqsanger.gz
	SRR10954104.fastq.gz	Fastqsanger.gz

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

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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

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Project description:Sexual dimorphism in mice

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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.

2022-11-21 | PXD038255 |

Sexual dimorphism in osteogenic differentiation

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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.

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