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Methylprednisolone selectively affects dystrophin expression in human muscle cultures

Day Laboratory for Neuromuscular Research. Massachusetts General Hospital and Harvard Medical School, Charlestown, MA.

Glucocorticoid therapy slows the progression of Duchenne muscular dystrophy. In muscle cultures, the addition of the glucocorticoid methylprednisolone increases myogenesis in most normal mixed and clonal cultures. Conversely, in some normal clonal and most dystrophic cultures, methylprednisolone inhibits fusion. However, in fusion-arrested normal and Becker muscular dystrophy cultures, dystrophin is expressed independently of fusion and of myosin heavy chain expression, and in some cases, expression is apparently enhanced by methylprednisolone. We suggest that dystrophin is a muscle-specific protein that does not require fusion for expression, and the methylprednisolone-induced enhancement of dystrophin expression may account for some of the clinical benefits of glucocorticoids in vivo.

Address correspondence and reprint requests to Dr. Orla Hardiman, Department of Physiology, University College Dublin, Earlsfort Terrace, Dublin 2, Ireland.

Supported by an American Academy of Neurology Fellowship in Neuropharmacology to O.H.; R.S. and R.H.B. were supported by a grant from the Cecil B. Day Investment Company. Support was also received from NIH grant RO1 00787–05 (R.H.B.), the Muscular Dystrophy Association, and the Pierre L. de Bourgknecht ALS Research Foundation.

Received May 12, 1992. Accepted for publication in final form July 15, 1992.

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