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A Comparison of Long-Term Survival of Muscle Precursor Cell Suspensions and Minced Muscle Allografts in the Non-Tolerant Mouse

  • Diana J. Watt
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 280)

Abstract

The recent discovery that the myopathic state of muscle fibres manifest in both the Duchenne and Becker forms of muscular dystrophy, is due to a deficiency or defect in the protein dystrophin (Hoffman et al., 1988; Arahata et al., 1988), supports the idea of treating recessively inherited diseases of skeletal muscle. By implanting normal muscle precursor cells, with a normal gene complement, into the multinucleate muscle fibres of affected individuals it should be possible to remedy this biochemical defect. In the experimental mouse model, we have already achieved a partial correction of an inherited biochemical defect of skeletal muscle by the introduction of grafts of muscle precursor cells into myopathic muscle deficient in the enzyme phosphorylase kinase (Morgan et al., 1988). More recently, Partridge et al., (1989), following the introduction of normal precursor cells into muscles of the X-linked Muscular Dystrophic (mdx) mouse which are normally deficient in dystrophin, have raised the levels of this protein by up to 30–40% of normal levels, indicating that a single injection of such precursor cells leads to synthesis of the missing gene product in substantial amounts.

Keywords

Muscular Dystrophy Single Cell Suspension Duchenne Muscular Dystrophy Myogenic Cell Adult Muscle 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Appleyard, S.T., Dunn, M.J., Dubowitz, V. and Rose, L.M. 1985. Increased expression of HLA ABC class 1 antigens by muscle fibres in Duchenne Muscular Dystrophy, inflammatory myopathy and other neuromuscular diseases. Lancet I: 361–363.CrossRefGoogle Scholar
  2. Arahata, K., Ishiura, S., Ishiguro, T., et al. 1988. Immunostaining of skeletal and cardiac muscle surface membrane with antibody against Duchenne muscular dystrophy peptide. Nature 333: 861–863.PubMedCrossRefGoogle Scholar
  3. Grounds, M.D., Partridge, T.A. and Sloper, J.C. 1980. The contribution of exogenous cells to regenerating skeletal muscle: An isoenzyme study of muscle allografts in mice. J. Path. 132: 325–341.PubMedCrossRefGoogle Scholar
  4. Gulati, A.K. and Zalewski, A.A. 1982. Muscle allograft survival after cyclosporin A immunosuppression. Exp. Neurol. 77: 378–385.PubMedCrossRefGoogle Scholar
  5. Hoffman, E.P. et al. 1988. Characterization of dystrophin in muscle-biopsy specimens from patients with Duchenne’s or Becker’s muscular dystrophy. New Engl. J. Med. 318: 1363–1368.PubMedCrossRefGoogle Scholar
  6. Karpati, G., Pouliot, Y. and Carpenter, S. 1988. Expression of immunoreactive major histocompatibility complex products in human skeletal muscles. Ann. Neurol. 23: 63–72.CrossRefGoogle Scholar
  7. Law, P.K., Goodwin, T.G. and Li, H-J. 1988. Histoincompatible myoblast injection improves muscle structure and function of dystrophic mice. Trans. Proc. 20: 1114–1119.Google Scholar
  8. Morgan, J.E., Watt, D.J., Sloper, J.C. and Partridge, T.A. 1988. Partial correction of an inherited biochemical defect of skeletal muscle by grafts of normal muscle precursor cells. J. Neurol. Sci. 86: 137–147.PubMedCrossRefGoogle Scholar
  9. Partridge, T.A. and Sloper, J.C. 1977. A host contribution to the regeneration of muscle grafts. J. Neurol. Sci. 33: 425–435.PubMedCrossRefGoogle Scholar
  10. Partridge, T.A., Grounds, M.D. and Sloper, J.C. 1978. Evidence of fusion between host and donor myoblasts in skeletal muscle grafts. Nature 273: 306–308.PubMedCrossRefGoogle Scholar
  11. Partridge, T.A., Morgan, J.E., Coulton, G.R., Hoffman, E.P. and Kunkel, L.M. 1989. Conversion of mdx myofibres from dystrophin-negative to -positive by injection of normal myoblasts. Nature 337: 176–178.PubMedCrossRefGoogle Scholar
  12. Ponder, B.A.J., Wilkinson, M.M., Wood, M. and Westwood, J.H. 1983. Immunohistochemical demonstration of H2 antigens in mouse tissue sections. J. Histochem. Cytochem. 31: 911–919.PubMedCrossRefGoogle Scholar
  13. Watt, D.J. 1982. Factors which affect the fusion of allogeneic muscle precursor cells in vivo. Neuropath. Appl. Neurol. 8: 135–147.CrossRefGoogle Scholar
  14. Watt, D.J., Partridge, T.A. and Sloper, J.C. 1981. Transplantation 31: 266–271.PubMedCrossRefGoogle Scholar
  15. Watt, D.J., Lambert, K., Morgan, J.E., Partridge, T.A. and Sloper, J.C. 1982. Incorporation of donor muscle precursor cells into an area of regeneration in the host mouse. J. Neurol. Sci. 57: 319–331.PubMedCrossRefGoogle Scholar
  16. Watt, D.J., Morgan, J.E. and Partridge, T.A. 1984a. Long term survival of allografted muscle precursor cells following a limited period of treatment with cyclosporin A. Clin. exp. Immunol. 55: 419–426.PubMedGoogle Scholar
  17. Watt, D.J., Morgan, J.E. and Partridge, T.A. 1984b. Use of mononuclear precursor cells to insert allogeneic genes into growing mouse muscles. Muscle and Nerve 7: 741–750.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Diana J. Watt
    • 1
  1. 1.Department of AnatomyCharing Cross and Westminster Medical SchoolLondonEngland

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