Exosomal miR-22-3p Derived from Chronic Rhinosinusitis with Nasal Polyps Regulates Vascular Permeability by Targeting VE-Cadherin

Figure 3

miR-22-3p directly targets VE-cadherin. (a) TargetScan software predicated that CDH5 (VE-cadherin) was a potential target of miR-22-3p. (b) Luciferase reporter vectors containing WT and MUT CDH5 3UTR were constructed. (c) Luciferase activity was significantly decreased in 293T cells cotransfected with the WT CDH5 3UTR vector and miR-22-3p, but was not significantly affected in cells cotransfected with the MUT CDH5 3UTR vector and miR-22-3p, relative to the control group. One-way ANOVA. and . (d) Representative IHC images of VE-cadherin in CRSwNP and IT tissues. VE-cadherin staining was mainly localized in the cytoplasm of cells. (e, f) Western blot of VE-cadherin expression in CRSwNP tissues. Student’s test. . (g) qRT-PCR of miR-22-3p expression in tissues. Student’s test. . (h) Pearson correlation between miR-22-3p and VE-cadherin expression. Linear correlation. (i, j) Western blot analysis and (k) qRT-PCR were used to measure the expression of VE-cadherin in HUVECs transfected with miR-22-3p-NC or miR-22-3p inhibitor. One-way ANOVA. and . (l–n) The expression of VE-cadherin at the protein and mRNA levels in HUVECs, respectively, cocultured with exosomes derived from pHNECs transfected with miR-22-3p-NC or miR-22-3p inhibitor. One-way ANOVA. and . Data are presented as of at least three independent experiments.

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