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RNA-sequencing explores the transcriptional profile of Wild Type and Fabp3-null mice under physiologicl and cardiac hypertrophic conditions

ABSTRACT: RNA-sequencing explores the transcriptional profile of Wild Type and Fabp3-null mice under physiologicl and cardiac hypertrophic conditions

PROVIDER: PRJNA736943 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14785851.fastq.gz	Fastqsanger.gz
	SRR14785852.fastq.gz	Fastqsanger.gz
	SRR14785853.fastq.gz	Fastqsanger.gz
	SRR14785854.fastq.gz	Fastqsanger.gz
	SRR14785855.fastq.gz	Fastqsanger.gz

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RNA-sequencing explores the transcriptional profile of Wild Type and Fabp3-null mice under physiologicl and cardiac hypertrophic conditions

Project description:Background: Cardiac hypertrophy was accompanied by various cardiovascular diseases (CVDs), due to the high global incidence and mortality of CVDs, it has become increasingly critical to characterize the pathogenesis of cardiac hypertrophy. We aimed to determine the metabolic effects of fatty acid binding protein 3 (FABP3), on transverse aortic constriction (TAC)-induced cardiac hypertrophy. Methods and Results: TAC or Ang II treatment markedly upregulated Fabp3 expression. Notably, Fabp3 ablation aggravated TAC-induced cardiac hypertrophy and cardiac dysfunction. Multi-omics analysis revealed that Fabp3-deficient hearts exhibited disrupted metabolic signatures characterized by increased glycolysis, toxic lipid accumulation, and compromised fatty acid oxidation and ATP production under hypertrophic stimuli. Mechanistically, FABP3 mediated metabolic reprogramming by directly interacting with PPARα, which prevented its degradation and synergistically modulated its transcriptional activity on Mlycd, Gck. Finally, treatment with the PPARα agonist, fenofibrate, rescued the pro-hypertrophic effects of Fabp3 deficiency.

2021-06-12 | GSE177041 | GEO

Human Cardiac Proteome of Hypertrophic Cardiomyopathy

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

2023-04-28 | MSV000091821 | MassIVE

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

Integrated proteomics unveils regulation of cardiac myocytes hypertrophic growth by a nuclear cAMP nanodomain under the control of PDE3A

Project description:Signalling by cAMP is organized in multiple distinct subcellular nanodomains regulated by cAMP-hydrolysing phosphodiesterase (PDEs). Cardiac b-adrenergic signalling has served as the prototypical system to elucidate cAMP compartmentalization. Here we employed an integrated interaction and phosphoproteomics approaches that take advantage of the unique role that individual PDEs play in the control of local cAMP to identify previously unrecognizedncAMP nanodomains associated with b-adrenegic stimulation. The characterization of one such domain demonstrated that PDE3A isoforms operate in a nuclear nanodomain that involves SMAD4 and HDAC-1 to inhibit cardiac myocyte hypertrophic growth.

2023-03-10 | PXD033773 | Pride

Cardiac reprogramming under defined conditions

Project description:FGF2, FGF10, and VEGF greatly promote cardiac reprogramming under defined serum-free conditions by enhancing the conversion of partially reprogrammed cells into fully reprogrammed functional iCMs. Fibroblasts can be directly reprogrammed into cardiomyocyte-like cells (iCMs) by overexpression of cardiac transcription factors, including Gata4, Mef2c, and Tbx5; however, this process is inefficient under serum-based culture conditions, in which the conversion of partially reprogrammed cells into fully reprogrammed functional iCMs has been a major hurdle. Here, we report that a combination of fibroblast growth factor (FGF) 2, FGF10, and vascular endothelial growth factor (VEGF), termed FFV, promoted cardiac reprogramming under defined serum-free conditions, increasing spontaneously beating iCMs by 100-fold compared with those under conventional serum-based conditions. Mechanistically, FFV activated multiple cardiac transcriptional regulators and converted partially reprogrammed cells into functional iCMs through the p38 mitogen-activated protein kinase and phosphoinositol 3-kinase/AKT pathways. Moreover, FFV enabled cardiac reprogramming with only Mef2c and Tbx5 through the induction of cardiac reprogramming factors, including Gata4. Thus, defined culture conditions promoted the quality of cardiac reprogramming, and this finding provides new insights into the mechanism of cardiac reprogramming.

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Altered Cardiac Energetics and Mitochondrial Dysfunction in Hypertrophic Cardiomyopathy

Project description:Altered Cardiac Energetics and Mitochondrial Dysfunction in Hypertrophic Cardiomyopathy

| PRJNA747806 | ENA

Phosphoproteomic analysis of cardiac biowires, cardiac hypertrophy patient explants, and hypertrophic mouse heart

Project description:we apply and evaluate an integrative mass spectrometry-based tissue profiling strategy that allows for a global quantitative phospho-proteomic survey of normal and disease tissue from human, mouse and OOC-derived specimens. The applicability and utility of this approach was tested in the context of fibrotic cardiac tissue samples from Biowire OOC specimens versus cardiac tissue surgical explants from hypertrophic patients and a transaortic constriction mouse pressure-overload model. Unique attributes and phosphorylation signatures specific to each tissue source were identified, but the results clearly showed that clinically-actionable biological inferences are generated by leveraging commonalities exhibited across the compendium. To validate the application of the cross-platform analytical framework, proof of principle drug testing was performed for selection of anti-fibrotic compounds targeting one of the identified fibrosis-related kinases, GSK3, consistent with a role as a key mediator of fibrosis.

2020-07-15 | PXD016492 | Pride

Parsing the roles of transcription factors Gata4 and Gata6 in adult cardiac hypertrophic responses

Project description:Cardiac hypertrophy is regulated by the zinc finger-containing DNA binding factors Gata4 and Gata6, both of which are required to mount a productive growth response of the adult heart. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response. We determined that Gata4 and Gata6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response itself following pressure overload stimulation. However, non-redundant functions were identified as functional decompensation induced by either Gata4 or Gata6 deletion was not rescued by the reciprocal transgene, and only Gata4 heart-specific deletion produced a reduction in capillary density after pressure overload. Gene expression profiling from hearts of these gene-deleted mice showed both overlapping and unique transcriptional codes, with Gata4 exhibiting the strongest impact. These results indicate that Gata4 and Gata6 play a dosage-dependent and semi-redundant role in programming cardiac hypertrophy, but that each has a unique role in maintaining cardiac homeostasis and adaptation to injury that cannot be compensated by the other. Microarray-bassed gene expression profiling identified overlapping, distinct, and quantitatively/differentially regulated classes of Gata4 or Gata6 regulated genes. To determine if Gata4 and Gata6 are redundant or have non-overlapping roles in programming cardiac hypertrophic responses and adaptation to stress or injury, we performed cardiomyocyte-specific conditional gene deletions for Gata4 and Gata6 in conjunction with reciprocal replacement with a transgene encoding either Gata4 or Gata6, during the pressure overload response.

2014-01-01 | E-GEOD-52317 | biostudies-arrayexpress

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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RNA-seq transcriptonal profiling in neonatal rat ventricular myocytes under hypertrophic growth

Project description:Heart failure is a leading cause of death in US. Hypertension is one of the most important risk factor of heart failure. In the presence of high blood pressure, the heart manifests hypertrophic growth to ameliorate ventricular wall stress. This once adaptive response may progress into decompensation and heart failure. The precise mechanisms governing this transition remain elusive. Here, we aimed to identify novel signaling pathways in cardiac hypertrophic growth. Primary neonatal rat ventricular myocytes (NRVMs) were isolated from 1-2 days old rats and treated with phenylephrine or IGF-1. Total RNA was isolated for RNA-seq analysis.

2020-11-16 | GSE153763 | GEO

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