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Fig. 4 | Respiratory Research

Fig. 4

From: Autophagy regulates the effects of ADSC-derived small extracellular vesicles on acute lung injury

Fig. 4

Autophagy inhibition weakened the inhibitory effect of ADSC-sEVs on LPS-induced PMVEC apoptosis and viability. A, B Typical flow cytometry quadrant diagrams and corresponding statistical analysis of apoptotic PMVECs. The top left, top right, and bottom right plots represent necrotic cells and late and early apoptotic cells, respectively. LPS markedly increased the percentage of endothelial cell apoptosis, which was effectively reduced by ADSC- sEVs. However, autophagy inhibition, significantly weakened the function of ADSC-sEVs (the percentage of endothelial cell apoptosis (%), control, 9.55 ± 1.96 vs. LPS, 52.73 ± 2.79 vs. LPS + ADSC-sEV, 21.73 ± 2.43 vs. LPS + ADSCsiATG5-sEV 34.57 ± 2.15). C, D Representative western blots and statistical analysis of Bax and Bcl-2 expression in PMVECs. LPS promoted the expression of Bax and reduced the expression of Bcl-2, ADSC- sEVs treatment inhibited the expression of Bax and promoted that of Bcl-2 under LPS stimulation. Autophagy inhibition weakened these effects of ADSC-sEVs (the relative expression of Bax, control, 0.52 ± 0.02 vs. LPS, 0.92 ± 0.03 vs. LPS + ADSC-sEV, 0.64 ± 0.04 vs. LPS + ADSCsiATG5-sEV, 0.74 ± 0.04. the relative expression of Bcl-2, control, 0.94 ± 0.04 vs. 0.61 ± 0.02 vs. LPS + ADSC-sEV, 0.85 ± 0.05 vs. LPS + ADSCsiATG5-sEV, 0.71 ± 0.02). The results are expressed as the mean ± SD of three independent experiments

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