Figure 4.

Skipping efficiency is increased dramatically when PMO is injected systemically at 4 days after CTX injury in WT mice. (A) Experimental model of the intramuscular injection of f-PMO into BL6 WT mice. f-PMO (400 µg/kg body weight) was injected into the CTX-injured TA muscles of mdx52 mice at Day 4 and the TA muscles analyzed 2 h after the injection of f-PMO. (B) Hematoxylin and eosin (H&E) staining (left) and immunofluorescence imaging of injured TA muscle for the detection of f-PMO (right). (C) Experimental model of the systemic intravenous injection of PMO into WT mice. Day 0 is defined as 5 weeks of WT mice. CTX was injected into the TA muscles of WT mice at Day 0. Between Day 0 and Day 6, PMO (320 mg/kg) was injected intravenously via tail vein into WT mice that had already received a CTX injection into TA muscles. RT–PCR analysis was performed 2 weeks after the PMO injection, respectively. (D) Detection of exon 51-skipped dystrophin mRNA by RT–PCR. Data are representative of four independent experiments. (E) Quantitative analysis by RT–PCR of exon 51 skipping by PMO. The percentages of skipped bands in each lane of (E) are shown. The data (n = 4) are presented as mean ± SD. *P < 0.05 and ***P < 0.001.