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. 2018 Jun 12;17(4):e12794. doi: 10.1111/acel.12794

Figure 4.

Figure 4

miR‐31a‐5p inhibition rejuvenates the aging phenotype of BMSCs via the E2F2 pathway. (a and d) Representative images of SA‐β‐gal staining in BMSCs transfected with miR‐31a‐5p mimics, miR‐31a‐5p inhibitor, or their controls were presented. (b and e) Overexpression or inhibition of miR‐31a‐5p in BMSCs was confirmed by γH2AX and H3K9me3 immunostaining. (c and f) The protein expression levels of E2F2 were reduced by the miR‐31a‐5p mimics and increased by miR‐31a‐5p suppression in BMSCs. (g) The potential binding sites for miR‐31a‐5p on the 3′UTR of E2F2. (h) 293T cells were transfected with a luciferase reporter vector containing either the WT or mutant plasmid of the 3′UTR of E2F2. (i) E2F2 protein was measured by Western blot and (j) miR‐31a‐5p inhibition significantly reduced SA‐β‐gal‐positive cells in si‐E2F2 treated BMSCs. # p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001. Scale bars: 100 μm (a, d and j); 4 μm (b and e). Data are presented as the mean ± SD, n = 3