setting is still unclear. We hypothesized that the inflammatory microenvironment prevents
cardioprotection mediated by endothelial cell (EC)-derived extracellular vesicles. The effects
of naïve EC-derived EV (eEV) or eEV released in response to interleukin-3 (IL-3)(eEV-IL-3)
were evaluated in cardiomyoblasts (H9c2) and rat hearts. In transwell assay, eEV protected
the H9c2 exposed to hypoxia/reoxygenation (H/R) more efficiently than eEV-IL-3 …