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SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [single-cell RNA-seq]

ABSTRACT: SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [single-cell RNA-seq]

PROVIDER: PRJNA797391 | ENA |

REPOSITORIES: ENA

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	SRR17622069.fastq.gz	Fastqsanger.gz
	SRR17622070.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [single-cell RNA-seq]

Project description:We established an efficient strategy to derive functional human SAN like pacemaker cells for disease modeling and drug screening. We used a dual-reporter cell line(SHOX2-GFP+MYH6-mcherry) to indicate the sinoatrial nodal like pacemaker cells. We sorted out the double positive cell population after Day20 and prepared the sample for single cell RNA seq analysis.

2022-01-26 | GSE193723 | GEO

SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells

Project description:SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells

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SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [bulk RNA-seq]

Project description:We established an efficient strategy to derive functional human SAN like pacemaker cells for disease modeling and drug screening. And we found SARS-CoV-2 infection causes dysfunction of human SAN like pacemaker cells and induces ferroptosis. And we also found that Deferoxamine and imatinib can block SARS-CoV-2 infection and infection-associated ferroptosis. Our study using functional human SAN like pacemaker cells demonstrates a potential mechanism for some COVID-19 cardiac abnormalities and identifies candidate drugs to protect the SAN like pacemaker from SARS-CoV-2 infection.

2022-01-26 | GSE193722 | GEO

Single-cell transcriptome analysis reveals CD34 as a marker of human sinoatrial node pacemaker cardiomyocytes [hPSC_SAN]

Project description:The sinoatrial node regulates the heart rate throughout life. Failure of this primary pacemaker results in life-threatening, slow heart rhythm. Despite its important function, the cellular and molecular composition of the human sinoatrial node is not resolved. Particularly, no cell surface marker to identify and isolate sinoatrial node pacemaker cells has been reported. Here we use single-nuclei/cell RNA sequencing of fetal and human pluripotent stem cell-derived sinoatrial node cells and show that they consist of three subtypes of pacemaker cells, including Core Pacemaker, Sinus Venosus, and Transitional Cells. Our study identifies a host of sinoatrial node pacemaker markers including MYH11, BMP4, and the cell surface antigen CD34. We demonstrate that sorting for CD34+ cells from stem cell differentiation cultures enriches for sinoatrial node cells with a functional pacemaker phenotype. This sinoatrial node pacemaker cell surface marker is highly valuable for stem cell-based disease modelling, drug discovery, cell replacement therapies, as well as the delivery of therapeutics to sinoatrial node cells in vivo using antibody-drug conjugates.

2024-10-30 | GSE279631 | GEO

Single-cell transcriptome analysis reveals CD34 as a marker of human sinoatrial node pacemaker cardiomyocytes [CITE-seq]

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Single-cell transcriptome analysis reveals CD34 as a marker of human sinoatrial node pacemaker cardiomyocytes [fetal SAN]

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SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [bulk RNA-seq]

Project description:SARS-CoV-2 Infection Induces Ferroptosis of Human Pluripotent Stem Cell-Derived Sinoatrial Nodal like Pacemaker Cells [bulk RNA-seq]

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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

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Project description:Each heartbeat is triggered by the sinoatrial node (SAN), the primary pacemaker of the heart. Studies in animal models have revealed that pacemaker cells share a common progenitor with the (pro)epicardium, and that the pacemaker cardiomyocytes further diversify into “transitional”, “tail” and “head” subtypes. However, the underlying molecular mechanisms, especially of human pacemaker cell development are poorly understood. Here, we performed single cell RNA sequencing (scRNA-seq) and trajectory inference on human induced pluripotent stem cells (hiPSCs) differentiating to SAN-like cardiomyocytes (SANCM) to construct a roadmap of transcriptional changes and lineage decisions. In differentiated SANCM, we identified distinct clusters that closely resemble different subpopulations of the in vivo SAN. Moreover, the presence of a side population of proepicardial cells suggested their shared ontogeny with SANCM, as also reported in vivo. Our results demonstrate that the divergence of SANCM and proepicardial lineages is determined by WNT signaling. Furthermore, we uncovered roles for TGFβ and WNT signaling in the branching of transitional and head SANCM subtypes, respectively. These findings provide new insights into the molecular processes involved in human pacemaker cell differentiation, opening new avenues for complex disease modeling in vitro and inform approaches for cell-therapy based regeneration of the SAN.

2022-09-01 | GSE189782 | GEO

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