Skip to main content
. 2018 Jan 29;14(3):404–418. doi: 10.1080/15548627.2017.1414755

Figure 4.

Figure 4.

The MIR30D-ATG5 axis plays an important role in the EndoMT. (A and B) Transduction of HBMECs with MIR30D lentivirus significantly inhibited the LPS-induced decreases in the TJP expression levels (A) and increases in the mesenchymal cell marker expression (B). HBMECs were transduced with the MIR30D lentivirus for 24 h and were subsequently incubated with LPS (10 ng/ml) for 24 h. All data are presented as the mean ± SD of 3 independent experiments. *P<0.05, **P<0.01, ***P<0.001 vs. the MIRCon group. #P<0.05, ##P<0.01, ###P<0.001 vs. the LPS-treated MIRCon group via one-way ANOVA followed by the Holm-Sidak test. (C and D) Transduction of HBMECs with the ATG5 siRNA significantly inhibited the decreases in the TJP expression levels (C) and the increases in the mesenchymal cell marker expression (D) induced by anti-MIR30D. HBMECs were cotransduced with anti-MIRCon or anti-MIR30D and either control siRNA or ATG5 siRNA for 24 h. All data are presented as the mean ± SD of 3 independent experiments. *P<0.05, **P<0.01 vs. the anti-MIRCon group with the control siRNA. #P<0.05, ##P<0.01 vs. the anti-MIR30D cotransduced with the control siRNA via one-way ANOVA followed by the Holm-Sidak test.