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J Biol Chem, Vol. 274, Issue 31, 21908-21912, July 30, 1999

Calcineurin Is Required for Skeletal Muscle Hypertrophy

Shannon E. Dunn, Jennifer L. Burns, and Robin N. Michel

From the Department of Chemistry and Biochemistry, Neuromuscular Research Laboratory, Laurentian University, Sudbury, Ontario P3E 2C6, Canada

Molecular signaling pathways linking increases in skeletal muscle usage to alterations in muscle size have not been identified. In the present study, we tested the hypothesis that calcineurin, a calcium-regulated phosphatase recently implicated in the signaling of some forms of cardiomyopathic growth, is required to induce skeletal muscle hypertrophy and muscle fiber type conversions associated with functional overload in vivo. Administration of the specific calcineurin inhibitors cyclosporin (CsA) or FK506 to mice, for which the fast plantaris muscle was overloaded for 1-4 weeks, prevented the rapid doubling of mass and individual fiber size and the 4-20-fold increase in the number of slow fibers that characterize this condition. CsA treatment influenced the expression of muscle myofibrillar protein genes in a way reflective of fiber phenotype transformations but only in the long term of the overload condition, suggesting that the control of this growth response by calcineurin is not limited to the transcriptional activation of these muscle-specific genes. Clinically, these results provide insight to the post-surgical muscle wasting and weakness observed in recovering transplant recipients administered therapeutic dosages of these immunosuppressants.


Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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