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. 2021 Nov 22;10(11):1854. doi: 10.3390/antiox10111854

Figure 7.

Figure 7

MiR-92b-3p over-expression reversed intermittent hypoxia with re-oxygenation (IHR)-induced apoptosis, monoamine oxidase (MAO)-A hyperactivity, and up-regulation of its target mRNAs through directly targeting PTGS1. Transfection with a miR-92b-3p mimic in THP-1 cells reversed IHR-induced (A) early apoptosis. Transfection with miR-92b-3p in HUVEC reversed IHR-induced up-regulation of its target genes, including (B) NF-κB1, and (C) PTGS1. Transfection with miR-92b-3p in SH-SY5Y cells reversed IHR-induced (D) ROS production, (E) early apoptosis, and (F) MAOA hyperactivity. (G) The wild-type sequence and mutated sequence of putative miR-92b-3p binding sites in the 3′untranslated region of PTGS1 are shown. (H) The direct binding between miR-92b-3p and PTGS1 was confirmed using luciferase reporter gene assays. * p < 0.05, compared with normoxic (NOX) condition. ** p < 0.01, compared with normoxic (NOX) condition. *** p < 0.001, compared with NOX condition. # p < 0.05, compared with IHR condition.