Cells, Volume 10, Issue 1
January 2021 - 194 articles
Cover Story: The role of extracellular vesicles (EV) in I/R settings remains controversial. This is particularly true for EV released by endothelial cells (EC) at the site of inflammation. Herein, the impact and the potential mechanisms of action of naïve EC-derived EV (eEV) and eEV released in response to interleukin-3 (IL-3) (eEV-IL-3) were explored in an I/R setting. We demonstrated that eEV, unlike eEV-IL-3, displays cardioprotective properties by activating the mitogen-activated protein kinase kinase (MEK1/2)/eNOS/guanylyl-cyclase (GC) pathways and by boosting antiapoptotic signals involving the B-cell-lymphoma-2 (Bcl-2) protein. Overall, our study demonstrated that the inflammatory cytokine IL-3 changes the eEV protein cargo and hampers eEV-mediated cardioprotection by transferring caveolin 1, as well as inflammatory and apoptosis cues. The role of extracellular vesicles (EV) in I/R settings remains controversial. This is particularly true for EV released by endothelial cells (EC) at the site
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