@entity1375 prolongs and increases mdx muscle precursor proliferation and delays myotube formation in normal and XXXX .

@entity1 @entity1375 @entity6415 @entity19 @entity1555 @entity5652 @entity121 @entity4497
@entity1375 (induced by 8 weeks of oral 0.05% @entity5652 ) heightened the phenotype of mdx @entity19 dystrophin-deficient @entity121 to more closely resemble @entity1 @entity1555 . Muscle repair after crush injury to the tibialis anterior muscle (TA) in @entity1375 mdx @entity19 showed decreased myotube formation and delayed debris removal. To investigate whether reduced muscle precursor cell proliferation can account for the effects of @entity1375 on repair from injury, immunocytochemistry for @entity4497 ( @entity4497 ) on muscle precursor cells and autoradiography to detect DNA synthesis were performed in control and mdx TA. The proportions of labelled @entity6415 ( @entity6415 ), @entity6415 ( @entity6415 ), and total mononuclear cell nuclei (TLN, the majority being muscle precursors) were counted in defined areas of regenerating TA after 2 and 4 days recovery. @entity6415 and the numbers of activated satellite cell nuclei on intact fibers were counted in surviving areas. In the same muscle, earlier phases of regeneration were observed in areas distal than proximal to the injury. At 2 days of regeneration, labelled @entity6415 were increased in treated compared with untreated mdx TA. In distal areas at 4 days, fewer muscle precursors had recently fused to myotubes in treated than in untreated mdx. In proximal areas 4 days (relatively late in repair), TLN data suggested that muscle precursor proliferation was greater in @entity1375 compared with untreated mdx TA. @entity4497 immunostaining was consistent with proliferation data and confirmed that there were more muscle precursors in mdx than in control regenerating muscle. These results suggest that @entity1375 prolongs and increases the phase of replication by mdx muscle precursors and delays precursor fusion into myotubes in regeneration.
