Muscular dysgenesis is a mutation which is characterized by paralysis of skeletal muscle cells. Excitation-contraction coupling is deficient and muscle cells display atypical ultrastructure. In vitro, mutant myotubes recover a normal phenotype when co-cultured with spinal cord cells from normal animals or with normal fibroblasts. We have shown that other types of cells, eg certain glial cells present in the spinal cord or in other tissues, have this capacity. In contrast, intervention of neurons in the recovery does not appear likely. Very different types of non-myoblastic cells, then, are capable of restoring contractile activity of dysgenic myotubes in vitro, suggesting that a non-specific mechanism is involved in the phenotypic reversion of affected muscle cells. The restoration process seems to imply a close relationship between myotubes and normal glial cells.

Functional and structural recovery of myotubes from mice with muscular dysgenesis after co-culture with normal, non-myoblastic cells

MELONE, Mariarosa Anna Beatrice;
1995

Abstract

Muscular dysgenesis is a mutation which is characterized by paralysis of skeletal muscle cells. Excitation-contraction coupling is deficient and muscle cells display atypical ultrastructure. In vitro, mutant myotubes recover a normal phenotype when co-cultured with spinal cord cells from normal animals or with normal fibroblasts. We have shown that other types of cells, eg certain glial cells present in the spinal cord or in other tissues, have this capacity. In contrast, intervention of neurons in the recovery does not appear likely. Very different types of non-myoblastic cells, then, are capable of restoring contractile activity of dysgenic myotubes in vitro, suggesting that a non-specific mechanism is involved in the phenotypic reversion of affected muscle cells. The restoration process seems to imply a close relationship between myotubes and normal glial cells.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/234835
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