Neuronal control of myogenic regulatory factor accumulation in fetal muscle.

The lumbosacral spinal cords of 14.5-day gestation mice (E14.5) were ablated.

Nonmuscle stem cells fail to significantly contribute to regeneration of normal muscle.

Whole, normal extensor digitorum longus muscles (EDL) were orthtopically transplanted into transgenic mice, expressing nuclear localing beta-galactosidase (nlsbeta-gal) under control of a muscle-specific promoter, in order to determine the extent to which nonmuscle derived, multipotent stem cells (which under experimental conditions exhibit myogenic potential) are spontaneously recruited from distal, nonmuscle organs to participate in the graft's regeneration. The host's contribution to the graft's regeneration was determined by evaluating the number and distribution of beta-gal positive myonuclei in regenerated grafts. Fibers with beta-gal positive nuclei accounted for approximately 1% of the long-term (28- and 56-day) graft's myofibers.

Aberrant development of motor axons and neuromuscular synapses in MyoD-null mice.

Myogenic regulatory factors (MRFs), muscle-specific transcription factors, are implicated in the activity-dependent regulation of nicotinic acetylcholine receptor (AChR) subunit genes. Here we show, with immunohistochemistry, Western blotting, and electron microscopy that MyoD, a member of the MRF family, also plays a role in fetal synapse formation. In the diaphragm of 14.

Immune response to full-length dystrophin delivered to Dmd muscle by a high-capacity adenoviral vector.

Adenoviral vector-mediated gene transfer to skeletal muscle is a promising potential treatment for Duchenne muscular dystrophy. However, the immunological response to viral antigens and the therapeutic protein expressed by the delivered gene could prevent effective treatment. In this study, we investigated the immune response induced by adenoviral and dystrophin antigens presented by high-capacity adenoviral vector-mediated dystrophin and beta-galactosidase delivery to skeletal muscle of a mouse model that is both dystrophin-deficient and lacZ transgenic.

Effect of injecting primary myoblasts versus putative muscle-derived stem cells on mass and force generation in mdx mice.

It is well established that the injection of normal myoblasts or of muscle-derived stem cells (MDSCs) into the muscle of dystrophin-deficient mdx mice results in the incorporation of a number of donor myoblasts into the host muscle. However, the effect of the injected exogenous cells on mdx muscle mass and functional capacity has not been evaluated. This study evaluates the mass and functional capacity of the extensor digitorum longus (EDL) muscles of adult, male mdx mice that received intramuscular injections of primary myoblasts or of MDSCs (isolated by a preplating technique; Qu, Z.