Journal
JOURNAL OF EXTRACELLULAR VESICLES
Volume 10, Issue 9, Pages -Publisher
WILEY
DOI: 10.1002/jev2.12117
Keywords
endothelial injury; inflammation; SARS-CoV-2; thrombosis
Categories
Funding
- National Institute of Health [R01DA042715, R01HL129875]
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The protein cargo in EVs can distinguish the severity of COVID-19, with enrichment of proinflammatory, procoagulation, immunoregulatory, and tissue-remodeling proteins. These proteins induce apoptosis of pulmonary microvascular endothelial cells.
Coronavirus disease-2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has lead to a global pandemic with a rising toll in infections and deaths. Better understanding of its pathogenesis will greatly improve the outcomes and treatment of affected patients. Here we compared the inflammatory and cardiovascular disease-related protein cargo of circulating large and small extracellular vesicles (EVs) from 84 hospitalized patients infected with SARS-CoV-2 with different stages of disease severity. Our findings reveal significant enrichment of proinflammatory, procoagulation, immunoregulatory and tissue-remodelling protein signatures in EVs, which remarkably distinguished symptomatic COVID-19 patients from uninfected controls with matched comorbidities and delineated those with moderate disease from those who were critically ill. Specifically, EN-RAGE, followed by TF and IL-18R1, showed the strongest correlation with disease severity and length of hospitalization. Importantly, EVs from COVID-19 patients induced apoptosis of pulmonary microvascular endothelial cells in the order of disease severity. In conclusion, our findings support a role for EVs in the pathogenesis of COVID-19 disease and underpin the development of EV-based approaches to predicting disease severity, determining need for patient hospitalization and identifying new therapeutic targets.
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