Fig. 5
From: Autophagy regulates the effects of ADSC-derived small extracellular vesicles on acute lung injury
Autophagy mediated the protective effect of ADSC-sEVs on LPS-induced PMVEC viability. A, B Representative fluorescence images and statistical analysis of LPS-induced endothelial cell death after incubation with sEVs derived from ADSC in the presence or absence of autophagy inhibition. LPS treatment significantly increased the percentage of dead cells, which were characterized by PI staining of the nuclei. Small extracellular vesicle pretreatment markedly alleviated LPS-induced cell death. However, autophagy inhibition markedly weakened sEV-mediated abrogation of cell death [the percentage of dead cells (%), control, 7.67 ± 1.27 vs. LPS, 33.57 ± 2.20 vs. LPS + ADSC-sEV, 21.67 ± 1.72 vs. LPS + ADSCsiATG5-sEV, 29.30 ± 1.51]. C MTT assays assessing the viability of PMVECs after LPS challenge. LPS significantly reduced cell viability, which was apparently alleviated by ADSC-sEVs. Autophagy inhibition reduced the effect of sEVs [the cell viability (OD), control, 2.94 ± 0.06 vs. LPS, 1.46 ± 0.21 vs. LPS + ADSC-sEV, 2.01 ± 0.14 vs. LPS + ADSCsiATG5-sEV, 1.49 ± 0.06]. The results are expressed as the mean ± SD of three independent experiments