The most widespread animal model to investigate Duchennemuscular dystrophy is the mdx-mouse. In contrast to humans, phases\nof muscle degeneration are replaced by regeneration processes; hence there is only a restricted time slot for research. The aim\nof the study was to investigate if an intramuscular injection of BTX-A is able to break down muscle regeneration and has direct\nimplications on the gene expression ofmyosin heavy chains in the corresponding treated and untreatedmuscles. Therefore, paralysis\nof the right massetermuscle was induced in adult healthy and dystrophic mice by a specific intramuscular injection of BTX-A. After\n21 days themRNA expression and protein content ofMyHC isoforms of the right and leftmasseter, temporal, and the tonguemuscle\nwere determined using quantitative RT-PCR andWestern blot technique.MyHC-IIa andMyHC-I-mRNA expression significantly\nincreased in the paralyzed masseter muscle of control-mice, whereas MyHC-IIb and MyHC-IIx/d-mRNA were decreased. In\ndystrophic muscles no effect of BTX-A could be detected at the level of MyHC. This study suggests that BTX-A injection is a\nsuitable method to simulate DMD-pathogenesis in healthy mice but further investigations are necessary to fully analyse the BTX-A\neffect and to generate sustained muscular atrophy in mdx-mice.
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