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

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

PROVIDER: PRJNA1142437 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30051391_1.fastq.gz	Fastqsanger.gz
	SRR30051391_2.fastq.gz	Fastqsanger.gz
	SRR30051392_1.fastq.gz	Fastqsanger.gz
	SRR30051392_2.fastq.gz	Fastqsanger.gz
	SRR30051393_1.fastq.gz	Fastqsanger.gz

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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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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.

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

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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.

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