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. 2016 Aug 18;6:31918. doi: 10.1038/srep31918

Figure 2. HMGN2 was the potential target of miR-155 and miR-23a to involve in regulating K. pneumoniae adhesion.

Figure 2

(A) Schematic presentation of base pairing between the 3′ UTR of HMGN2 and miR-155 or miR-23a by erect likes. The mutant seed sequence of the HMGN2 3′ UTR matching miR-23a is also presented by dots. (B) Western blot analysis showing the change of HMGN2 protein level in K. pneumoniae infected A549 and HBE16 cells at different infection time (MOI = 100). (C) Western blot analysis showing the effect of miR-23a mimic on the protein expressions of HMGN2 in K. pneumoniae infected A549 or HBE16 cells (MOI = 100 for 2 hours, same as D–F). (D) Western blot analysis showing the effect of miR-155 mimic or inhibitor on the protein expressions of HMGN2 in K. pneumoniae infected or uninfected cells. (E) A549 cells were co-transfected with miR-23a mimic or miR-NC along with HMGN2 3′ UTR wild-type (WT) or mutant (MUT) reporter. Luciferase activity was measured 24 hr after transfection. (F) The relative K. pneumoniae adhesion in A549 cells co-transfected with pEx-HMGN2 and miR-155 or miR-23a mimic. (Data are the mean ± SD and represent three individual experiments. **p < 0.01 compared with miR-NC and pEx-NC cotransfection).