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. 2021 Nov 3;27:16–36. doi: 10.1016/j.omtn.2021.10.024

Figure 6.

Figure 6

Silencing lncRNA AAB by NM + si-AAB + MSN reverses the ferroptosis of CMEC

(A) Illustration of the targeted recognition of NM + si-AAB + MSN, cellular uptake within a CMEC, intracellular cell membrane dissociation, MSN degradation, and siRNA release. (B) lncRNA AAB expression level was determined by qRT-PCR in CMECs treated with the NM + si-AAB + MSN for 48 h at different siRNA doses. Data are represented by means ± SEM (n = 6). #p < 0.05 and ##p < 0.01 versus 0 nM. (C and D) Cell viability of CMECs induced by Ang II for 24 h was detected after treatment with si-AAB, si-AAB + MSN, and NM + si-AAB + MSN, respectively. (E) Immunofluorescence results of PECAM-1 in CMECs. (F) The miR-30b-5p mRNA level in CMECs. (G and H) Western blot analysis of TIMP1, MMP9, and TFR-1 in CEMCs. (I) Statistical analysis chart of iron ions content. (J) Immunofluorescence results of ROS in CMECs of different groups. (K) Statistical analysis chart of MDA content. (L) qRT-PCR analysis of the expression level of ptgs2 mRNA in CMECs. (M) Statistical analysis of CMEC mortality. Ang II group: CMECs were treated with 100 nM Ang II for 24 h following by treatment with PBS for 48 h. si-AAB group: CMECs were given 100 nM Ang II for 24 h following by treatment with si-AAB for 48 h. si-AAB + MSN group: CMECs were given 100 nM Ang II for 24 h following by treatment with si-AAB + MSN for 48 h. NM + si-AAB + MSN group: CMECs were given 100 nM Ang II for 24 h following by treatment with NM + si-AAB + MSN for 48 h. Data are represented by means ± SEM (n = 6). ##p < 0.01 versus control group; ∗p < 0.05 and ∗∗p < 0.01 versus Ang II group. Scale bars, (D) 10 μm; (E and J) 50 μm.