Inhibition of muscle cell development in culture by cells from spinal cord due to production of low molecular weight factor

Kagen, Lawrence J.; Collins, Kim D.; Roberts, Louis A.; Butt, Andrew

doi:10.1016/0012-1606(76)90042-7

Cited by 10 publications

(2 citation statements)

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“…The inhibitor was produced in smaller quantities by skin and lung fibroblasts. These results are difficult to relate to other studies in which nerve and muscle cells have been grown together (see Section V) but examination of figure z b (Kagen et al, 1976) suggests that their nerve-cell preparations consisted of fibroblasts and glia-like cells only. If these latter cells were responsible for the myogenic inhibitor, purified cultures of nerve cells should be used and DNA inhibitors such as aminopterin (Fischback, 1972) have been used to kill fibroblasts and glial cells.…”

Section: ( D ) Growth Factorsmentioning

confidence: 58%

“…In contrast with studies using brain extracts, Kagen, Collins, Roberts & Butt (1976) found that dissociated chick embryonic spinal cord cells that had been in culture for 4 days released a low molecular factor into the culture medium that inhibited myogenesis of chick embryonic muscle cell. The inhibitor was produced in smaller quantities by skin and lung fibroblasts.…”

Section: ( D ) Growth Factorsmentioning

confidence: 58%

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Diseased Muscle Cells in Culture

Witkowski

1977

Biological Reviews

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Summary (1) Cultures of differentiated muscle cells have been grown from diseased human, mouse and chick skeletal muscle, and from cardiac muscle of the myopathic hamster. (2) Methods of culture established for normal embryonic and adult skeletal muscle cells have proved suitable for cultures of diseased muscle cells. (3) Myoblasts obtained from dy2J mouse muscle crushed in vivo before explanting fuse in culture and form morphologically normal myotubes. Studies of the effects of innervation by dy2J spinal cord neurones on the differentiation of normal, dy2J and dy myotubes have been inconclusive but it is probable that innervation does not play a part in the pathogenesis of this disorder. (4) Myoblasts prepared by trypsinization of embryonic dy muscle behave normally in culture and fuse to form myotubes that appear normal. It is not clear if myoblasts that migrate from explants of adult muscle in vitro fuse. Aggregates of non‐fusing cells have been described, but under other culture conditions normal and abnormal forms of myotube have been observed. dy muscle fibres fail to regenerate even when cultured with normal spinal cord explants and dy nerves are without effect on regenerating normal muscle fibres. These tissue‐culture studies suggest that the dy mouse mutation is a myopathic disorder. (5) Embryonic mdg myoblasts have a normal cell cycle in vitro and fuse to form well‐differentiated myotubes with cross‐striations. mdg myotubes have normal electro‐physiological properties but do not contract spontaneously or on depolarization. The defect in the muscle of the mdg mutant appears to be a failure of excitation‐contraction coupling. (6) Cells migrate earlier from explants of adult dystrophic chick muscle than from normal muscle but dystrophic chick myotubes appear morphologically normal. Myotubes prepared from embryonic dystrophic chick muscle become vacuolated and degenerate, changes that can be prevented by anti‐proteases such as antipain. Lactic dehydrogenase isozyme subunit M4 is absent from dystrophic muscle in vivo but reappears in cultured myotubes. Dystrophic myotubes innervated in culture by either normal or dystrophic neurones exhibit bi‐directional lcoupling and multiple innervation. These results suggest that there are changes in dystrophic myotubes and that chick muscular dystrophy is a myopathy. (7) Cardiac muscle cells from the cardiomyopathic hamster synthesize less actin and myosin than normal cells, and Z lines in dystrophic cells are irregularly arranged. The beat frequency of myopathic cardiac cells is lower than that of normal cells and declines more rapidly. Tissue‐culture studies have not been made of hamster skeletal muscle. (8) Human dystrophic myotubes do not show degenerative changes in culture and have normal histochemical reactions. RNA synthesis appears normal in dystrophic myotubes but there may be changes in adenyl‐cyclase activity and protein synthesis in dystrophic cells. Morphological and biochemical changes have been found in muscle cells cultured from a case of acid‐maltase d...

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Section: ( D ) Growth Factorsmentioning

confidence: 58%

Section: ( D ) Growth Factorsmentioning

confidence: 58%

Diseased Muscle Cells in Culture

Witkowski

1977

Biological Reviews

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Early effects in vitro of the muscular dysgenesis mutation on nervous tissue in the mouse

Wieczorek

1984

Muscle and Nerve

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Muscular dysgenesis (mdg), a disease expressed in embryonic mice, severely affects the formation and differentiation of skeletal musculature. The focus of this investigation was an analysis of dysgenic nervous tissue with special attention centered on interactions between muscle and nerve cells in vitro. Results indicate that mdg/mdg spinal cord cells can form functional neuromuscular junctions in nerve-muscle cocultures and induce contractions in dysgenic muscle. However, dysgenic spinal cord cells induce fewer myotubes to contract and result in a delayed induction of dysgenic myotube contractile activity. Furthermore, mdg/mdg nervous tissue, or its conditioned medium, is associated with a higher incidence of morphologically abnormal myotube contractures. The results from this investigation demonstrate that there are functional abnormalities in both dysgenic muscle and nervous tissues which are stable and expressed for up to 3 weeks in vitro.

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