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Articles in PresS, published online ahead of print January 30, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00424.2001
Submitted on September 4, 2001
Accepted on January 29, 2002
1 Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA
2 Anatomy and Neurobiology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
3 Geriatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Central Arkansas Veterans Health Care System, Little Rock, AR, USA
* To whom correspondence should be addressed. E-mail: dupontesthere{at}uams.edu.
In this study, the role of the calcineurin pathway in skeletal muscle atrophy and atrophy-reducing interventions was investigated in rat soleus muscles. Since 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. Hind limb suspension and spinal cord transection were used to induce atrophy and intermittent reloading and exercise, respectively, were used to reduce atrophy. Cyclosporine (CsA) was administered at 25 mg/kg/day 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. Therefore, results suggest that calcineurin may be playing opposing roles during skeletal muscle atrophy and under muscle mass maintaining conditions.
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