Fig. 9
From: Autophagy regulates the effects of ADSC-derived small extracellular vesicles on acute lung injury
The effect of ADSC-sEVs with or without autophagy inhibition on toll-like receptor 4 (TLR4)-nuclear factor (NF)-κB signaling in LPS-triggered PMVECs. A Representative western blots showing expressions of TLR4, MyD88 and total or phosphorylated(p)- NF-κB p65. B Statistical analysis of the relative expressions level of TLR4, MyD88 and phosphorylated(p)- NF-κB p65. LPS promoted the expression of TLR4, MyD88 and phosphorylated(p)-NF-κB p65. ADSC-sEVs treatment decreased expressions of all the aforementioned proteins. Autophagy inhibition by siATG5, however, significantly weakened the effect of ADSC-sEVs on inhibiting the TLR4/NF-κB signaling related proteins (the relative expressions level of TLR4, control, 0.28 ± 0.01 vs. LPS, 1.19 ± 0.03 vs. LPS + ADSC-sEV, 0.62 ± 0.03 vs. ADSCsiATG5-sEV, 0.91 ± 0.02. the relative expressions level of phosphorylated(p)- NF-κB p65, control, 0.19 ± 0.01 vs. LPS 0.97 ± 0.04 vs. LPS + ADSC-sEV, 0.49 ± 0.02 vs. ADSCsiATG5-sEV, 0.79 ± 0.03. the relative expressions level of MyD88, control, 0.25 ± 0.02 vs. LPS 1.05 ± 0.01 vs. LPS + ADSC-sEV, 0.55 ± 0.02 vs. ADSCsiATG5-sEV, 0.77 ± 0.02). The results are expressed as the mean ± SD of three independent experiments