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Am J Physiol Cell Physiol 282: C1387-C1395, 2002. First published January 30, 2002; doi:10.1152/ajpcell.00424.2001
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Vol. 282, Issue 6, C1387-C1395, June 2002

Maintenance of muscle mass is not dependent on the calcineurin-NFAT pathway

Esther E. Dupont-Versteegden1, Micheal Knox1, Cathy M. Gurley1, John D. Houlé2, and Charlotte A. Peterson1,3

Departments of 1 Geriatrics and 2 Anatomy and Neurobiology, University of Arkansas for Medical Sciences, and 3 Central Arkansas Veterans Health Care System, Little Rock, Arkansas 72205

In this study, the role of the calcineurin pathway in skeletal muscle atrophy and atrophy-reducing interventions was investigated in rat soleus muscles. Because calcineurin has been suggested to be involved in skeletal and cardiac muscle hypertrophy, we hypothesized that blocking calcineurin activity would eliminate beneficial effects of interventions that maintain muscle mass in the face of atrophy-inducing stimuli. Hindlimb suspension and spinal cord transection were used to induce atrophy, and intermittent reloading and exercise were used to reduce atrophy. Cyclosporin (CsA, 25 mg · kg-1 · day-1) was administered to block calcineurin activity. Soleus muscles were studied 14 days after the onset of atrophy. CsA administration did not inhibit the beneficial effects of the two muscle-maintaining interventions, nor did it change muscle mass in control or atrophied muscles, suggesting that calcineurin does not play a role in regulating muscle size during atrophy. However, calcineurin abundance was increased in atrophied soleus muscles, and this was associated with nuclear localization of NFATc1 (a nuclear factor of activated T cells). Therefore, results suggest that calcineurin may be playing opposing roles during skeletal muscle atrophy and under muscle mass-maintaining conditions.

cyclosporin; hindlimb suspension; spinal cord transection; soleus


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