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Quantitative proteomic and single-nucleus transcriptomics map of the sinus node elucidates the foundation of cardiac pacemaking

ABSTRACT: Quantitative proteomic and single-nucleus transcriptomics map of the sinus node elucidates the foundation of cardiac pacemaking

PROVIDER: PRJNA541019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9008740.fastq.gz	Fastqsanger.gz
	SRR9008750.fastq.gz	Fastqsanger.gz
	SRR9008741.fastq.gz	Fastqsanger.gz
	SRR9008732.fastq.gz	Fastqsanger.gz
	SRR9008742.fastq.gz	Fastqsanger.gz

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Quantitative proteomic and single-nucleus transcriptomics map of the sinus node elucidates the foundation of cardiac pacemaking

Project description:The sinus node is a collection of highly specialised cells constituting the heart’s pacemaker. It is keenly debated whether the so-called membrane or alternatively Ca2+ clocks provide the molecular substrate of pacemaking. By high-resolution mass spectrometry, we quantified >7,000 proteins from sinus node and neighbouring atrial muscle. The abundances of 575 proteins differed between the two tissues, including particular differences in metabolic profiles and extracellular matrix composition. Most notably, the data reveal significant differences between the tissues in the ion channels responsible for the membrane clock, but not in Ca2+ clock proteins, suggesting that the membrane clock underpins pacemaking. By performing single-nucleus RNA sequencing of sinus node biopsies, we attributed protein abundances to specific cell types. Consistent with these results, incorporation of the ion channel expression differences into a biophysically-detailed atrial action potential model resulted in pacemaking and a sinus node-like action potential. Combining our quantitative proteomics data with computational modeling, we estimate ion channel copy numbers for sinus node myocytes. Our findings provide detailed insights into the unique molecular make-up of the pacemaker of the heart.

2019-05-04 | GSE130710 | GEO

Quantitative proteomics profiling determines the uniqueness of the sinus node

Project description:The sinus node is a collection of highly specialized cells that constitute the natural pacemaker activity of our heart. The protein expression landscape of the sinus node differs from the surrounding cardiac tissue, although it is primarily comprised of myocytes and fibroblasts like the rest of the cardiac tissue, endowing it with its unique ability to regulate heart rate. Here we performed quantitative proteomics experiments to profile protein expression in the pacemaker of the heart, and compared it to protein expression in the neighbouring atrial muscle. In summary, the quantitative proteomics data presented here offer a highly detailed insight into the unique composition of the pacemaker of our heart.

2019-07-08 | PXD008736 | Pride

Proteomics Couples Electrical Remodeling to Inflammation in a Murine Model of Heart Failure with Sinus Node Dysfunction

Project description:In patients with heart failure, concomitant sinus node dysfunction (SND) is an important predictor of mortality, yet its molecular underpinnings are poorly understood. Here, we acquired deep sinus node proteomes and phosphoproteomes in mice with heart failure and SND and report extensive remodelling. Intersecting the measured (phospho)proteome changes with human genomics and pharmacovigilance data highlighted downregulated proteins involved in electrical activity such as the pacemaker ion channel, Hcn4. We confirmed the importance of ion channel downregulation for sinus node physiology using computer modelling. Guided by the proteomics data, we hypothesized that an inflammatory response may drive the electrophysiological remodeling underlying SND in heart failure. In support of this, experimentally induced inflammation downregulated Hcn4 and slowed pacemaking in the isolated sinus node. From the proteomics data we identified proinflammatory cytokine-like protein galectin-3 as a potential target to mitigate the effect. Indeed, in-vivo suppression of galectin-3 in the animal model of heart failure prevented SND. Collectively, we outline the protein and phosphorylation remodeling of SND in heart failure, we highlight a role for inflammation in electrophysiological remodelling of the sinus node, and we present galectin-3 signalling as a target to ameliorate SND in heart failure.

2024-04-25 | PXD031084 | Pride

Alectinib Induces Sinus Bradycardia through Inhibiting Cacna1d Expression, Mediating Electro-Dysfunction in Sinus Node

Project description:Alectinib is the first-line therapy for anaplastic lymphoma kinase rearranged non-small cell lung cancer. Sinus node bradycardia as a major adverse cardiac event still widely impact patient’s quality of life. However, the underlying mechanism of alectinib induce sinus bradycardia (AISB) remains elusive. The aim of this study was to reveal the pathogenesis of the AISB in a rat model including the electrophysiology alterations and the molecular basis

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Alectinib Induces Sinus Bradycardia through Inhibiting Cacna1d Expression, Mediating Electro-Dysfunction in Sinus Node

Project description:Alectinib Induces Sinus Bradycardia through Inhibiting Cacna1d Expression, Mediating Electro-Dysfunction in Sinus Node

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Quantitative proteomics and single-nucleus transcriptomics of the sinus node elucidates the foundation of cardiac pacemaking.

Project description:The sinus node is a collection of highly specialised cells constituting the heart's pacemaker. The molecular underpinnings of its pacemaking abilities are debated. Using high-resolution mass spectrometry, we here quantify >7,000 proteins from sinus node and neighbouring atrial muscle. Abundances of 575 proteins differ between the two tissues. By performing single-nucleus RNA sequencing of sinus node biopsies, we attribute measured protein abundances to specific cell types. The data reveal significant differences in ion channels responsible for the membrane clock, but not in Ca2+ clock proteins, suggesting that the membrane clock underpins pacemaking. Consistently, incorporation of ion channel expression differences into a biophysically-detailed atrial action potential model result in pacemaking and a sinus node-like action potential. Combining our quantitative proteomics data with computational modeling, we estimate ion channel copy numbers for sinus node myocytes. Our findings provide detailed insights into the unique molecular make-up of the cardiac pacemaker.

| S-EPMC6599035 | biostudies-literature

Gene expression profiling of lymph node sub-capsular sinus macrophages in cancer

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Mouse sinoatrial node transcriptome

Project description:RNA Sequencing of Mouse Sinoatrial Node Reveals an Upstream Regulatory Role for Islet-1 in Cardiac Pacemaker Cells Rationale: Treatment of sinus node disease with regenerative or cell-based therapies will require a detailed understanding of gene regulatory networks in cardiac pacemaker cells (PCs). Objective: To characterize the transcriptome of PCs using RNA sequencing, and to identify transcriptional networks responsible for PC gene expression. Methods and Results: We used laser capture micro-dissection (LCM) on a sinus node reporter mouse line to isolate RNA from PCs for RNA sequencing (RNA-Seq). Differential expression and network analysis identified novel SAN-enriched genes, and predicted that the transcription factor Islet-1 (Isl1) is active in developing pacemaker cells. RNA-Seq on SAN tissue lacking Isl1 established that Isl1 is an important transcriptional regulator within the developing SAN. Conclusions: (1) The PC transcriptome diverges sharply from other cardiomyocytes; (2) Isl1 is a positive transcriptional regulator of the PC gene expression program. There are 25 RNA-Sequencing Samples

2015-02-06 | E-GEOD-65658 | biostudies-arrayexpress

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Vibrio sinus

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