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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

ABSTRACT: Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

PROVIDER: PRJNA637572 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11934376_1.fastq.gz	Fastqsanger.gz
	SRR11934376_2.fastq.gz	Fastqsanger.gz
	SRR11934377_1.fastq.gz	Fastqsanger.gz
	SRR11934377_2.fastq.gz	Fastqsanger.gz
	SRR11934378_1.fastq.gz	Fastqsanger.gz

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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [scRNA-seq dataset]

Project description:Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [scRNA-seq dataset]

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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [bulk RNA-seq dataset)

Project description:Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [bulk RNA-seq dataset)

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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages [scRNA-seq dataset]

Project description:Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology is unknown. We examined heart tissue from autopsies of healthy and COVID-19 patients using RNA-seq and identified a strikingly increased CCL2 expression and macrophage population in COVID-19 heart sample. Transwell assays using hESC-derived cardiomyocytes (CMs) and macrophages revealed that SARS-CoV-2 infected CMs secrete CCL2, which recruits macrophages, and this was validated using adult human CMs. Macrophages recruited by CCL2 from infected CMs secrete IL-6 and TNF-α, which causes increased ROS and cell apoptosis of CMs. Finally, a high content chemical screen using FDA-approved drugs identified ranolozine and tofacitinib, which rescue SARS-CoV-2 infected CMs from macrophages-induced cardiotoxicity.

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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is predominantly defined by respiratory symptoms, but cardiac complications including arrhythmias, heart failure, and viral myocarditis are also prevalent. Although the systemic ischemic and inflammatory responses caused by COVID-19 can detrimentally affect cardiac function, the direct impact of SARS-CoV-2 infection on human cardiomyocytes is not well understood.

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profiling of histone modifications in SARS-CoV-2 infected cells

Project description:Purpose: The goal of this study is to understand the response and pathology of the epigenome upon infection with SARS-CoV-2 in lung and heart tissues Methods: AT2 and induced cardiomyocytes were infected (MOI 4) with SARS-CoV-2 or Mock infection control for 48 hours followed by chromatin immunoprecipitation and sequencing. Results: global differences in hPTMs were observed upon infection related to SARS-CoV-2 histone mimicry Conclusions: SARS-CoV-2 sucks

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