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. Author manuscript; available in PMC: 2008 Nov 8.
Published in final edited form as: Mol Ther. 2005 Feb;11(2):245–256. doi: 10.1016/j.ymthe.2004.09.013

FIG. 5.

FIG. 5

Adult (9-month-old) mdx EDL muscles were poorly transduced by AV.ΔR4/ΔC and minimally protected from eccentric contraction-induced injury. The left EDL muscles of 9-month-old mdx mice were infected with AV.ΔR4/ΔC. The contralateral right EDL muscles served as uninfected controls. Viral transduction and muscle contraction were examined at 3 months postinfection. (A) Representative photomicrographs of immunofluorescence staining with the N-terminal-specific (for ΔR4/ΔC microdystrophin, left) and the C-terminal-specific (for endogenous revertant murine dystrophin, right) antibodies. Scale bar, 300 μm. On average, approximately 32% of the EDL myofibers were transduced by AV.ΔR4/ΔC (Table 2). Revertant myofibers (arrow) were seen more frequently in older mice (right). (B) Limited microdystrophin expression in older mdx EDL muscles did not improve specific tetanic force. Open bar, uninfected EDL muscles; filled bar, AV.ΔR4/ΔC-infected muscles. N = 4 pairs. (C) Limited microdystrophin expression resulted in marginal protection against eccentric contraction-induced injury in the mdx EDL muscle (significant difference was seen only after the second and third stretch cycle). Open circle, uninfected EDL muscles (mean − SEM); closed circle, EDL muscles infected with AV.ΔR4/ΔC (mean + SEM). N = 4 pairs. *The difference between uninfected and AV.ΔR4/ΔC-infected muscles was statistically significant ( P < 0.05).