
| 10.1124/jpet.122.001209
http://scihub22266oqcxt.onion/10.1124/jpet.122.001209
 35772782!9827505!35772782
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J+Pharmacol+Exp+Ther 2023 ; 384 (1): 109-115 Nephropedia Template TP
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Exosomal miR-145 and miR-885 Regulate Thrombosis in COVID-19 #MMPMID35772782Gambardella J; Kansakar U; Sardu C; Messina V; Jankauskas SS; Marfella R; Maggi P; Wang X; Mone P; Paolisso G; Sorriento D; Santulli GJ Pharmacol Exp Ther 2023[Jan]; 384 (1): 109-115 PMID35772782show ga
We hypothesized that exosomal microRNAs could be implied in the pathogenesis of thromboembolic complications in coronavirus disease 2019 (COVID-19). We isolated circulating exosomes from patients with COVID-19, and then we divided our population in two arms based on the D-dimer level on hospital admission. We observed that exosomal miR-145 and miR-885 significantly correlate with D-dimer levels. Moreover, we demonstrate that human endothelial cells express the main cofactors needed for the internalization of the "Severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2), including angiotensin converting enzyme 2, transmembrane protease serine 2, and CD-147. Interestingly, human endothelial cells treated with serum from COVID-19 patients release significantly less miR-145 and miR-885, exhibit increased apoptosis, and display significantly impaired angiogenetic properties compared with cells treated with non-COVID-19 serum. Taken together, our data indicate that exosomal miR-145 and miR-885 are essential in modulating thromboembolic events in COVID-19. SIGNIFICANCE STATEMENT: This work demonstrates for the first time that two specific microRNAs (namely miR-145 and miR-885) contained in circulating exosomes are functionally involved in thromboembolic events in COVID-19. These findings are especially relevant to the general audience when considering the emerging prominence of post-acute sequelae of COVID-19 systemic manifestations known as Long COVID.|*COVID-19/complications[MESH]|*Exosomes/metabolism[MESH]|*MicroRNAs/genetics/metabolism[MESH]|*Post-Acute COVID-19 Syndrome/genetics/metabolism[MESH]|*Thrombosis/genetics/metabolism/virology[MESH]|Endothelial Cells[MESH]|Humans[MESH]
  
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