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Fig. 7 | Journal of Nanobiotechnology

Fig. 7

From: Hepatic small extracellular vesicles promote microvascular endothelial hyperpermeability during NAFLD via novel-miRNA-7

Fig. 7

Steatotic hepatocyte is a significant source of novel-miR-7-enriched sEV. Human hepatocyte cell line were treated with 100 μmol/L palmitic acid (PA) or vehicle for 18 h. Hepatocyte sEVs in the HepG2 cell culture media were collected by ultracentrifugation. Human microvascular endothelial cell line-1 (HMEC-1) was transfected with 100 nmol/L novel-miR-7 inhibitor or negative control (NC) inhibitor, and incubated with Ctrl-sEVs or PA-sEVs from HepG2 for 24 h. A HepG2, HuH7 and L02 were treated with 100 μmol/L PA or vehicle for 18 h. SEVs were collected from the supernatant and the expression levels of novel-miR-7 were measured by qPCR analysis, n = 4 per group. B Representative western blot bands and the summarized data determined by densitometric analysis, n = 4 per group. C Representative images of acridine orange (AO) and magic red (MR) staining, n = 4 per group. Scale bar, 20 μm. D Representative flow cytometry images of caspase-1 FLICA staining and the summarized data of the positive cells, n = 4 per group. The fold changes were obtained by calculating the ratio of the positive cells of the treated groups to the NC inhibitor group. E Relative permeability of the endothelial monolayer to FITC-dextran, n = 4 per group. Data are expressed as the mean ± SEM. Statistics: Student t-test (A) and One-way ANOVA (B, D, E), *P < 0.05, **P < 0.01 vs. vehicle group; &P < 0.05, &&P < 0.01 vs. NC inhibitor plus ctrl-sEVs group; $P < 0.05, $$P < 0.01 vs. NC inhibitor plus PA-sEVs

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