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Biomedical subjects

F Rieger

Publications and source records attributed to F Rieger.

158 records · Page 9Linked to original sources
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N-cadherin and N-CAM-mediated adhesion in development and regeneration of skeletal muscle.

In this review, the experimental evidence supporting the fact that the cell adhesion molecules N-CAM and N-cadherin are involved in myogenesis has been surveyed. In order to give access to the function of these molecules, a strategy of in vivo localization and in vitro perturbation of their adhesive function by interfering antibodies and peptides was applied. Both molecules are expressed at the surface of myogenic cells during myogenesis in vivo and in vitro. The blockade of the N-CAM adhesion function leads to a mild reduction of the rate of myoblast fusion, while the inhibition of the N-cadherin function induces a drastic inhibition of fusion suggesting that N-cadherin-mediated adhesion is a critical step in the process of myoblast fusion. Both molecules are re-expressed during muscle regeneration suggesting that adult myogenesis is under the control of the same adhesive systems as embryonic and foetal myogenesis.

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PubMedDate not supplied

Restoration of dysgenic muscle contraction and calcium channel function by co-culture with normal spinal cord neurons.

Muscular dysgenesis (mdg) is a spontaneous recessive lethal mutation in the mouse. The disease is characterized by a total lack of excitation-contraction coupling in embryonic skeletal muscle. This developmental abnormality is associated with a drastic deficiency in the expression of voltage-sensitive Ca2+ channels in skeletal muscle without alteration of the properties of voltage-sensitive Na+ channels or of voltage-sensitive Ca2+ channels in cardiac and neuronal cells. Membrane couplings between sarcoplasmic reticulum and the transverse tubules, known as triads, were also found to be drastically altered in embryonic muscle of the homozygous mutant (mdg/mdg). Triads in the mdg/mdg muscle were less numerous, disorganized and lacked spaced densities. This paper shows that co-culture of mdg/mdg myotubes with normal spinal cord neurons re-establishes Ca2+ channel activity, contraction and normal triad organization. The decrease thus cannot be due to a mutation of the Ca2+ channel as previously suggested. Normal nerve cells may supply an essential factor to mutant muscle cells.

Animals↗