Abstract
ObjectiveEpidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 μm, PM2.5) increases the morbidity and mortality of respiratory diseases. Emerging evidence suggests that human circulating extracellular vesicles (EVs) may offer protective effects against injury caused by particulate matter. Currently, however, whether EVs attenuate PM2.5-induced A549 cell apoptosis is unknown. MethodsEVs were isolated from the serum of healthy subjects, quantified via nanoparticle tracking analysis, and qualified by the marker protein CD63. PM2.5-exposed (50 μg/mL) A549 cells were pre-treated with 10 μg/mL EVs for 24 h. Cell viability, cell apoptosis, and AKT activation were assessed via Cell Counting Kit-8, flow cytometry, and Western blot, respectively. A rescue experiment was also performed using MK2206, an AKT inhibitor. ResultsPM2.5 exposure caused a 100% increase in cell apoptosis. EVs treatment reduced cell apoptosis by 10%, promoted cell survival, and inhibited the PM2.5-induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM2.5-exposed A549 cells. Moreover, EVs treatment reversed PM2.5-induced reductions in p-AKTThr308 and p-AKTSer473. AKT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM2.5-exposed A549 cells. ConclusionsEVs treatment promotes cell survival and attenuates PM2.5-induced cell apoptosis via AKT phosphorylation. Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM2.5-induced lung injury.
Published Version
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