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. 2016 Aug 2;5(8):e341. doi: 10.1038/mtna.2016.51

Figure 8.

Figure 8

Dystrophin exon-skipping and protein expression following i.m. administration of PMOE23 with polymers in TA muscle of mdx mice (aged 4–5 weeks) 2 weeks after treatment. Muscles were treated with PMOE23 (2 µg) and PEAs (10 µg) or PEI 25k (2 µg)/Endo-porter (5 µg) in 40 µl saline. PMOE23 (2 µg) only was used as control: (a) Restoration of dystrophin in TA muscle was detected by immunohistochemistry with rabbit polyclonal antibody P7. Blue nuclear staining with DAPI (4,6-diamidino-2-phenylindole). (scale bar = 200 µm). (b) The percentage of dystrophin-positive fibers in a single cross-section induced by PMOE23 with/without polymer formulation (mean ± SD, n = 5, Student's t-test, *P ≤ 0.05 compared with PMOE23). (c) Detection of exon 23 skipping by RT-PCR. Total RNA (100 ng) of from each sample was used for amplification of dystrophin mRNA from exon 20 to exon 26. The upper bands (indicated by E22+E23+E24) correspond to the normal mRNA and the lower bands (indicated by E22+E24) correspond to the mRNA with exon E23 skipped. (d) Western blot demonstrates the expression of dystrophin protein from treated mdx mice compared with C57BL/6 and untreated mdx mice. Dys: dystrophin detected with a monoclonal antibody ManDys 1. α-Actin was used as the loading control.