Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

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

Authors: Dupont-Versteegden, EE  Knox, M  Gurley, CM  Houle, JD  Peterson, CA 
Citation: Dupont-Versteegden EE, etal., Am J Physiol Cell Physiol 2002 Jun;282(6):C1387-95.
Pubmed: (View Article at PubMed) PMID:11997253
DOI: Full-text: DOI:10.1152/ajpcell.00424.2001

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 x kg(-1) x 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.


Gene Ontology Annotations
Objects Annotated
Objects referenced in this article

Additional Information

CRRD Object Information
CRRD ID: 628398
Created: 2003-01-02
Species: All species
Last Modified: 2003-01-02
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.