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. 2022 Apr 15;2022:5517648. doi: 10.1155/2022/5517648

Figure 6.

Figure 6

NEAT1 delivered by BMSC-EVs induces proliferation and autophagy of chondrocytes but represses their apoptosis via the miR-122-5p/Sesn2 axis. (a) Sesn2 mRNA expression in chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 detected by RT-qPCR. (b) Proliferation of chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 detected by CCK-8. (c) Apoptosis of chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 measured by flow cytometry. (d) Autophagy of chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 measured by MDC staining. (e) Formation of autophagosomes and autolysosome in chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 analyzed by mRFP-GFP-LC3 double fluorescence assay. (f) Beclin-1 and LC3-II/I mRNA expression in chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 analyzed by RT-qPCR. (g) Beclin-1 protein expression and the ratio of LC3-II/I in chondrocytes treated with Lv-NEAT1-BMSC-EVs or combined with sh-Sesn2 analyzed by Western blot analysis. ∗p < 0.05. Measurement data were expressed as mean ± standard deviation. Data among groups were compared by one-way ANOVA followed by Tukey's post hoc test. Data at different time points were compared using repeated-measures ANOVA followed by Bonferroni's post hoc test. The cell experiment was run in triplicate independently.