Fig. 7: CEC-EVs-derived miR-672-5p promoted autophagy and suppressed NLRP3 inflammasome activation. | Cell Death & Disease

Fig. 7: CEC-EVs-derived miR-672-5p promoted autophagy and suppressed NLRP3 inflammasome activation.

From: Cerebral endothelial cell-derived extracellular vesicles regulate microglial polarization and promote autophagy via delivery of miR-672-5p

Fig. 7

A CEC-EVs-derived miR-672-5p enhances LC3II, Beclin1 level and decreases SQSTM1/p62 expression. B–D Statistical graphs of protein expression of LC3II, Beclin1 and SQSTM1/p62. E Immunofluorescence staining of microglial cells transfected with mRFP-GFP-LC3 adenovirus. F, G Calculated numbers of autophagosome (GFP+ RFP+ yellow puncta) and autolysosome (red puncta) numbers. All data are present as means ± SD (n = 3). One-way ANOVA. **p < 0.01 compared to Control group. ##p < 0.01 compared to LPS group. &&p < 0.01 compared to LPS + miR-NCKD-EVs group. H, I Chloroquine (CQ) was used to evaluate the effects of CEC-EVs treatment or LPS treatment on LC3II. CEC-EVs-derived miR-672-5p alleviates LPS-induced microglial inflammatory responses (J) and activation (K). All data are present as means ± SD (n = 6). One-way ANOVA. *p < 0.05, **p < 0.01 compared to CQ− group. ##p < 0.01 compared to CQ+ group.

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