Screening of muscle regenerative molecules for Duchenne muscular dystrophy

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The MRL mouse shows complete closure of ear punch wounds. However, genetic and molecular mechanisms underlying the accelerated wound healing have remained largely unknown. We have mated dystrophin-deficient mdx mice with MRL mice to generate and characterize MRL-introduced mdx mice. Compared to the mdx mice, the MRL-mdx mice showed increased myofiber size and centrally-nucleated myofiber number, but decreased fibrosis in the diaphragm. By comparing the gene expression profile in diaphragm between mdx and MRL-mdx mice, we found several candidate genes contributing to the MRL-originated muscle regeneration. Among them, two genes eventually accelerating myotube formation in cultured myoblasts. Our results suggest that the introduction of the MRL wound-healer accelerates muscle regeneration by reducing muscle fibrosis, thereby becoming a novel therapeutic option for the dystrophin-deficient muscular dystrophy.