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AN INVESTIGATION OF THE INFLUENCE OF THE EXTRACELLULAR ENVIRONMENT ON THE REGENERATION OF THE NORMAL AND DYSTROPHIC MOUSE MUSCLE IN VITRO
Author(s) -
WEST M. R.,
PARSONS R.
Publication year - 1980
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1980.tb00289.x
Subject(s) - regeneration (biology) , biology , explant culture , extracellular , muscular dystrophy , anatomy , myocyte , muscle tissue , in vitro , skeletal muscle , microbiology and biotechnology , andrology , pathology , medicine , biochemistry , genetics
West M.R. & Parsons R. 1980 Neuropathology and Applied Neurobiology 6,181–194 An investigation of the influence of the extracellular environment on the regeneration of the normal and dystrophic mouse muscle in vitro The regenerative response of normal and dystrophic muscle cultured with fetal spinal cord has been investigated. Nearly all the normal muscle explants regenerated, but the dystrophic muscle gave a much more varied response as only 30% regenerated, and 38% showed total explant degradation with loss of all recognisable muscle elements. Forty‐five % of the dystrophic explants, produced ‘pseudostraps’ in which there was an apparent block of myoblast fusion. Cultures in which cellular contact between spinal cord tissue and the normal or dystrophic muscle was prevented showed less regeneration than when it was allowed. However, the incidence of regeneration in these cultures was much higher than when the muscle was cultured in isolation. Direct cellular contact between the cord and the muscle is, therefore, not necessary to initiate regeneration which is presumably mediated in these cultures by changes in the chemical environment. This is substantiated by the almost complete absence of regeneration in cultures of muscle alone, where the fibres were shown to be devoid of nuclei within 5 days. The experiments have shown that under our conditions, a myogenic defect is apparent in the dystrophic muscle. This does not exlude a possible neuronal involvement in the aetiology of the disease, although we have no evidence to support it.