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At least 883 records · Page 49Linked to original sources
PubMed2002

Androgen receptor enhances myogenin expression and accelerates differentiation.

Animal and clinical studies indicated that the androgen-AR signaling pathway is required for appropriate development of sexually dimorphic skeletal muscles and increases lean muscle mass, muscle strength, and muscle protein synthesis. However, the detailed mechanisms by which the androgen-AR signaling pathway regulates skeletal muscle development need further study at the molecular level. C2C12 myoblast cells stably transfected with the Flag-tagged AR were used to analyze the role of androgen-AR signaling pathway in skeletal muscle development. The results indicate that the androgen-AR signaling pathway may suppress skeletal myoblast cell growth and accelerate myoblast cell differentiation via enhanced myogenin expression. This is a first report showing the role of androgen-AR signaling pathway in regulation of myoblast cell growth and myogenic regulatory factors.

Animals↗
PubMed1986

Embryonic myosin heavy chain as a differentiation marker of developing human skeletal muscle and rhabdomyosarcoma. A monoclonal antibody study.

Hybridoma cell lines were obtained from the fusion of NS-O myeloma cells with spleen cells of mice immunized with bovine fetal skeletal myosin. A stable hybridoma clone, BF-G6, produced immunoglobulin G1 k antibodies reacting specifically with embryonic-type myosin heavy chains present in fetal but not in neonatal or adult human skeletal muscle, as determined by enzyme immunoassay and immunoblot analysis. Fetal but not adult skeletal muscle fibers were stained by this monoclonal antibody in indirect immunofluorescence assays; smooth muscle cells and cardiac muscle cells, as well as non-muscle cells were also unreactive. Solid tumors of infants and children were tested for reactivity with BF-G6 by immunofluorescence and immunoperoxidase staining. Embryonic myosin heavy chain was expressed in rhabdomyosarcomas but not in other types of tumor, except for Wilms' tumor. Rhabdomyosarcoma cells isolated from a bone marrow metastasis and grown in vitro for several months were also labelled by BF-G6. Embryonic myosin heavy chain can thus be used as a specific differentiation marker of normal and neoplastic skeletal muscle tissue.

Adolescent↗
PubMed1983

Effect of denervation at birth on the development of skeletal muscle cell types in the rat.

In the newborn rat all cells of soleus, extensor digitorum longus (EDL), and tibialis anterior (TA) muscles stained for fast troponin I. A proportion of the cells, that was much higher in the soleus, also stained for slow troponin I. Fast and slow troponin I were segregated in different cell types in all three muscles 10 to 12 days after birth. No subsequent changes in the distribution of the two forms of troponin I occurred with further growth of EDL and TA muscles. The number of type I cells in soleus steadily increased with increasing age to 24 weeks. Three weeks after denervation at birth, almost all cells in soleus muscle stained for fast troponin I but less than 5% stained significantly dark for slow troponin I. All cells stained for myosin ATPase after alkaline preincubation, but very few after acid preincubation. Three weeks after denervation of EDL and to a lesser extent with TA muscle, fast and slow troponin I were still segregated in different cells. After alkaline preincubation all cells stained equally dark for myosin ATPase but only those positive for slow troponin I stained for myosin ATPase after acid preincubation.

Animals↗
PubMed1990

Sarcolemmal K+ channel activity in developing rat skeletal muscle membranes.

A method has been adapted to produce membrane vesicles suitable for routine membrane patch clamping from neonate rat skeletal muscle. Single K+ channel activity was recorded from cell-free inside-out patches. Most Ca2(+)-activated voltage sensitive channels had large conductances of up to 300 pS, as determined from their current/voltage relationship, and an open probability (Po) approaching unity at positive membrane potentials. A lower conductance K+ channel, probably responsible for inward rectification, had a lower conductance of about 100 pS. Outward rectifying K+ channels were also observed with the lowest conductance, about 40 pS. 0.1 mM ATP when applied to the inner membrane surface reduced or blocked activity, drastically reducing Po without altering single channel conductance. Such an effect has been reported in other preparations but was different in the neonate preparation in that it blocked channels with conductances as high as 300 pS. The simple preparation described, which we have also used successfully on mature rat and mouse skeletal muscle, has potential in the analysis of channel activities in various conditions and pathologies without the need for tissue culture to produce suitable membrane preparations.

Adenosine Triphosphate↗