Human Serum-derived Extracellular Vesicles Protect A549 from PM 2.5 -induced Cell Apoptosis.

Autor: Zhou QL; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China;Shanghai Applied Radiation Institute, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China., Bai YZ; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China., Gao J; School of Medicine, Shanghai University, Shanghai 200444, China., Duan Y; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China., Lyu YC; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China., Guan LF; China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing 101149, China., Elkin K; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA., Xie YL; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China., Jiao Z; Shanghai Applied Radiation Institute, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China., Wang HY; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Jazyk: angličtina
Zdroj: Biomedical and environmental sciences : BES [Biomed Environ Sci] 2021 Jan 20; Vol. 34 (1), pp. 40-49.
DOI: 10.3967/bes2021.006
Abstrakt: Objective: Epidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 μm, PM 2.5 ) 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 PM 2.5 -induced A549 cell apoptosis is unknown.
Methods: EVs were isolated from the serum of healthy subjects, quantified via nanoparticle tracking analysis, and qualified by the marker protein CD63. PM 2.5 -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.
Results: PM 2.5 exposure caused a 100% increase in cell apoptosis. EVs treatment reduced cell apoptosis by 10%, promoted cell survival, and inhibited the PM 2.5 -induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM 2.5 -exposed A549 cells. Moreover, EVs treatment reversed PM 2.5 -induced reductions in p-AKT Thr308 and p-AKT Ser473 . AKT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM 2.5 -exposed A549 cells.
Conclusions: EVs treatment promotes cell survival and attenuates PM 2.5 -induced cell apoptosis via AKT phosphorylation. Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM 2.5 -induced lung injury.
(Copyright © 2020 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.)
Databáze: MEDLINE
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