Regeneration after cardiotoxin injury of innervated and denervated slow and fast muscles of mammals

Myosin isoform analysis

Authors

  • Anne d'ALBIS,

    Corresponding author
    1. Laboratoire de Biologie Physicochimique, Unité 1131 Associée au Centre National de la Recherche Scientifique, Université Paris-Sud, Orsay
    Search for more papers by this author
  • René COUTEAUX,

    1. Institut des Neurosciences du Centre National de la Recherche Scientifique, Département de Cytologie, Université Pierre et Marie Curie, Paris
    Search for more papers by this author
  • Chantal JANMOT,

    1. Laboratoire de Biologie Physicochimique, Unité 1131 Associée au Centre National de la Recherche Scientifique, Université Paris-Sud, Orsay
    Search for more papers by this author
  • Agnès ROULET,

    1. Laboratoire de Biologie Physicochimique, Unité 1131 Associée au Centre National de la Recherche Scientifique, Université Paris-Sud, Orsay
    Search for more papers by this author
  • Jean-Claude MIRA

    1. Institut des Neurosciences du Centre National de la Recherche Scientifique, Département de Cytologie, Université Pierre et Marie Curie, Paris
    2. Laboratoire de Neurobiologie, Université René Descartes, Paris
    Search for more papers by this author

Correspondence to A. d'Albis, Laboratoire de Biologie Physicochimique, Bâtiment 433, Université Paris-Sud, F-91405 Orsay, France

Abstract

The regeneration of adult rat and mouse slow (soleus) and fast (sternomastoid) muscles was examined after the degeneration of myofibers had been achieved by a snake venom cardiotoxin, under experimental conditions devised to spare as far as possible the satellite cells, the nerves, and the blood vessels of the muscles.

Three days after the injury, no myosin was detectable in selected portions of the muscles. New myosins of embryonic, neonatal, and adult types started to be synthesized during the following two days. Adult myosins thus appeared more precociously than in development, which implies that the synthesis of myosin isoforms during regeneration does not entirely ‘recapitulate’ the sequence of myosin transitions observed during normal development.

Two weeks after the injury, the isomyosin electrophoretic pattern displayed by regenerated muscles was already the same as that of control muscles; the normal adult pattern was therefore expressed more rapidly in regenerating than in developing muscles.

Except for the synthesis of the slow isoform which was generally inhibited in denervated muscles, the same types of myosins were expressed during the early stages of regeneration in denervated as in innervated muscles; long-term denervation prevented however the qualitative and quantitative recovery of the normal myosin pattern.

Ancillary