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

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

PROVIDER: PRJNA637579 | 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 [bulk RNA-seq dataset)

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

| PRJNA637580 | ENA

Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

Project description:Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

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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 [bulk RNA-seq dataset)

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Cardiomyocytes Infected by SARS-CoV-2 Recruit Cardiotoxic Macrophages

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Cardiotoxic effects of mycotoxin citrinin on mammalian cells revealed by transcriptome profiling

Project description:Mycotoxin citrinin (CTN) is widely found in multiple types of grains in foods and feeds globally. CTN also contaminates Monascus-derived health supplements such as red yeast rice and red yeast extracts during the fermentation process, which are originally used for preventing cardiovascular diseases. A previous study has reported that CTN is cardiotoxic to zebrafish embryos during their development by interfering some cardiogenic genes and pathways, showing a potential risk of consuming CTN-contaminated foods and products. However, the cardiotoxic effects and the underlying mechanisms of CTN on mammalian cardiomyocytes remain unclear and need to be ellucidated. In this study, we performed RNA-seq experiments in order to investigate the transcriptomic alterations induced by CTN-exposed rat H9c2 cardiomyocytes. The transcriptome profiling we obtained may reveal some evidence regarding the toxic effects of CTN on cardiac phenotypes, chromosome segregation, tubulin arrangement, mitochondrial functioning, and stress responses, etc.

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Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2.

Project description:Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology remains unknown. Here, using an established in vivo hamster model, we demonstrate that SARS-CoV-2 can be detected in cardiomyocytes of infected animals. Furthermore, we found damaged cardiomyocytes in hamsters and COVID-19 autopsy samples. To explore the mechanism, we show that both human pluripotent stem cell-derived cardiomyocytes (hPSC-derived CMs) and adult cardiomyocytes (CMs) can be productively infected by SARS-CoV-2, leading to secretion of the monocyte chemoattractant cytokine CCL2 and subsequent monocyte recruitment. Increased CCL2 expression and monocyte infiltration was also observed in the hearts of infected hamsters. Although infected CMs suffer damage, we find that the presence of macrophages significantly reduces SARS-CoV-2-infected CMs. Overall, our study provides direct evidence that SARS-CoV-2 infects CMs in vivo and suggests a mechanism of immune cell infiltration and histopathology in heart tissues of COVID-19 patients.

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