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SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression

ABSTRACT: SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression

PROVIDER: PRJNA803375 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17883257.fastq.gz	Fastqsanger.gz
	SRR17883258.fastq.gz	Fastqsanger.gz
	SRR17883259.fastq.gz	Fastqsanger.gz
	SRR17883260.fastq.gz	Fastqsanger.gz
	SRR17883261.fastq.gz	Fastqsanger.gz

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SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression

Project description:In the initial process of COVID-19, SARS-CoV-2 infects respiratory epithelial cells and then transfers to other organs via the blood vessels. It is believed that SARS-CoV-2 can pass the vascular wall by altering the endothelial barrier using an unknown mechanism. In this study, we investigated the effect of SARS-CoV-2 on the endothelial barrier using an airway-on-a-chip that mimics respiratory organs and found that SARS-CoV-2 produced from infected epithelial cells disrupts the barrier by decreasing Claudin-5 (CLDN5), a tight junction protein, and disrupting vascular endothelial cadherin (VE-cadherin)-mediated adherens junctions. Consistently, the gene and protein expression levels of CLDN5 in a COVID-19 patient’s lungs were decreased. CLDN5 overexpression or Fluvastatin treatment could rescue the SARS-CoV-2-induced respiratory endothelial barrier disruption. We therefore concluded that the downregulation of CLDN5 expression is a pivotal mechanism for SARS-CoV-2-induced endothelial barrier disruption in respiratory organs and that inducing CLDN5 expression is a novel therapeutic strategy against COVID-19.

2022-09-22 | GSE196113 | GEO

SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression.

Project description:In the initial process of coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects respiratory epithelial cells and then transfers to other organs the blood vessels. It is believed that SARS-CoV-2 can pass the vascular wall by altering the endothelial barrier using an unknown mechanism. In this study, we investigated the effect of SARS-CoV-2 on the endothelial barrier using an airway-on-a-chip that mimics respiratory organs and found that SARS-CoV-2 produced from infected epithelial cells disrupts the barrier by decreasing Claudin-5 (CLDN5), a tight junction protein, and disrupting vascular endothelial cadherin-mediated adherens junctions. Consistently, the gene and protein expression levels of CLDN5 in the lungs of a patient with COVID-19 were decreased. CLDN5 overexpression or Fluvastatin treatment rescued the SARS-CoV-2-induced respiratory endothelial barrier disruption. We concluded that the down-regulation of CLDN5 expression is a pivotal mechanism for SARS-CoV-2-induced endothelial barrier disruption in respiratory organs and that inducing CLDN5 expression is a therapeutic strategy against COVID-19.

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SARS-CoV-2 disrupt respiratory vascular barrier by suppressing Claudin-5 expression (additional RNA-seq data)

2022-09-22 | GSE206635 | GEO

SARS-CoV-2 disrupt respiratory vascular barrier by suppressing Claudin-5 expression (additional RNA-seq data)

Project description:SARS-CoV-2 disrupt respiratory vascular barrier by suppressing Claudin-5 expression (additional RNA-seq data)

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