The contractile apparatus of striated muscle in the course of atrophy and regeneration

Jakubiec-Puka, Anna; Kulesza-Lipka, D; Kordowska, Jolanta

doi:10.1007/bf00204794

Cited by 17 publications

(7 citation statements)

References 18 publications

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“…The occurrence of phagocytes is probably due to removal of fiber remnants. This description seems to be in accordance with the events that have been shown during atrophy caused by denervation (20,34,39) and tenotomy (2). The degenerative changes in immobilized muscles were shown at the ultrastructural level to be most severe in red muscle fibers (12,58).…”

Section: Ultrastructural Aspects Of Immobilization Atrophysupporting

confidence: 88%

“…Several approaches have been made in the past to determine the cellular mechanisms and the biochemical changes during muscle atrophy. Beyond experimental immobilization, muscles were denervated (13,20,34,39,43,49,50,51,55) or tenotomy was used to reduce their activity (2,3,4,15,47). As Lippmann and Selig (41) pointed out, the results obtained by denervation or tenotomy may not be compared with immobilized muscles since in the first case the afferent impulses are blocked preventing the occurrence of muscular reflexes and in the latter case the muscle is artificially shortened.…”

Section: Introductionmentioning

confidence: 99%

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Skeletal Muscle Atrophy During Immobilization

Appell¹

1986

Int J Sports Med

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Section: Ultrastructural Aspects Of Immobilization Atrophysupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Skeletal Muscle Atrophy During Immobilization

Appell¹

1986

Int J Sports Med

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“…Denervation atrophy or recovery of the denervated muscle following reinnervation was produced under ether anaesthesia by, respectively, cutting or crushing the sciatic nerve, as previously described in detail [12, 131. After crushing the sciatic nerve, atrophy of the rat leg muscles progresses for about 15 days at the same rate as that produced by cutting the nerve. After this time, recovery of the muscle begins owing to reinnervation [5,131. Full recovery from denervation atrophy of most muscle characteristics (including normal histochemical pattern without type-grouping) takes about 4 months; the muscle then looks quite normal [12].…”

Section: Experiments On Ratsmentioning

confidence: 99%

Myosin heavy chain isoform composition in striated muscle after denervation and self‐reinnervation

Jakubiec-Puka

Kordowska

Catani³

et al. 1990

European Journal of Biochemistry

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The total content of myosin heavy chains (MHC) and their isoform pattern were studied by biochemical methods in the slow-twitch (soleus) and fast-twitch (extensor digitorum longus) muscles of adult rat during atrophy after denervation and recovery after self-reinnervation. The pattern of fibre types, in terms of ultrastructure, was studied in parallel.After denervation, total MHC content decreased sooner in the slow-twitch muscle than in the fast-twitch. The ratio of MHC-1 and the MHC-2B isoforms to the MHC-2A isoform decreased in the slow and the fast denervated muscles, respectively. After reinnervation of the slow muscle, the normal pattern of MHC recovered within 10 days and the type 1 isoform increased above the normal. In the reinnervated fast muscle, the 2B/2A isoform ratio continued to decrease. Traces of the embryonic MHC isoform, identified by immunochemistry, were found in both denervated and reinnervated slow and fast muscles. A shift in fibre types was similar to that found in the MHC isoforms. Within 2 months of recovery a tendency to normalization was observed.The results show that (a) MHC-2B isoform and the morphological characteristics of the 2B-type muscle fibres are susceptible to lack of innervation, similar to those of type 1, (b) during muscle recovery induced by reinnervation the MHC isoforms and muscle fibres shift transiently to type 1 in the soleus and to type 2A in the extensor digitorum longus muscles, and (c) the embryonic isoform of MHC may appear in the adult skeletal muscles if innervation is disturbed.During the last decade, plasticity of the striated muscle has been intensively studied (results are summarized in [l -31) and the general rules of denervation atrophy and of reinnervation recovery are well known. However, it is not fully understood how in the mature striated muscle a disturbed innervation influences remodelling of the contractile apparatus. We would like to stress that in the slow leg muscle (in adult rats) atrophying after denervation, the myosin filaments disappear before the actin filaments [4] ; simultaneously the muscle content of myosin heavy chains (MHC) decreases considerably. After reinnervation, when the muscle begins to recover, its MHC content increases rapidly in parallel with recovery of the correct proportion and arrangement of thin and thick filaments [4, 51. Nevertheless, it is not known how the total content of MHC changes in the denervated and reinnervated fast muscle.Myosin polymorphism is characteristic of different types of skeletal muscle fibres. The isoform composition of myosin may become adapted to modifications of functional requirements (for review see [6, 71). In chronically denervated mixed muscles (2 -6 months after the operation) expression of the fast isoform of myosin prevails, while after a long-term reinnervation (6 months of recovery) myosin composition is simi- lar to that of the normal muscle [8, 91. On the other hand, it is not clear how the myosin isoforms change in the shortterm denervated muscle and whether any lack of inne...

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“…Denervation of skeletal muscle causes extensive changes in its morphological, biochemical, and physiological characteristics. The main reason for these alterations, commonly referred to as "atrophic," is the interruption of neuron-muscle interaction (Sellin et al, 1980;Kabara and Tweedle, 1981;Jakubiec-Puka et al, 1981;Salonen et al, 1985;Czyzewski et al, 1985). These drastic changes in skeletal muscle after denervation are likely to be'reflected in the ability of skeletal muscle to regenerate after injury.…”

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confidence: 99%

Long‐term reiention of regenerative capability after denervation of skeletal muscle, and dependency of late differentiation on innervation

Gulati

1988

Anat. Rec.

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The present study examines the influence of denervation on the regenerative ability of skeletal muscle in rats. Muscle denervation was achieved by transecting and ligating the cut ends of the sciatic nerve. Four to 48 weeks after denervation, the extensor digitorum longus (EDL) muscle was autotransplanted to induce muscle regeneration. The transplanted EDL muscles were examined at 1-12 weeks. Normal (i.e., no prior denervation) EDL muscle autotransplants were also examined for comparison. Denervation resulted in progressive atrophy of muscle, marked by a reduction in the size of myofibers and an increase in endomysialperimysial connective tissue. In spite of these alterations, typical events of muscle regeneration were invariably observed after transplantation. Initial myofiber degeneration and subsequent regeneration of myotubes occurred in a manner similar to normal muscle transplants. However, only a partial maturation of myotubes was observed in denervated muscles. These results show that extended denervation does not abolish the capability for muscle regeneration. The precursor myosatellite cells, proposed to be responsible for muscle regeneration, retain their regenerative potential after denervation. It is concluded, however, that the presence of intact innervation is crucial for the terminal differentiation and maturation of regenerating muscle.

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The contractile apparatus of striated muscle in the course of atrophy and regeneration

Cited by 17 publications

References 18 publications

Skeletal Muscle Atrophy During Immobilization

Skeletal Muscle Atrophy During Immobilization

Myosin heavy chain isoform composition in striated muscle after denervation and self‐reinnervation

Long‐term reiention of regenerative capability after denervation of skeletal muscle, and dependency of late differentiation on innervation

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