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Am J Physiol Regul Integr Comp Physiol (August 31, 2006). doi:10.1152/ajpregu.00561.2006
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Submitted on August 8, 2006
Accepted on August 30, 2006

Burn-Induced Increase in Atrogin-1 and MuRF-1 in Skeletal Muscle is Glucocorticoid-Independent but Down Regulated by IGF-I

Charles H. Lang1*, Danuta Huber1, and Robert A. Frost1

1 Cell Molec Physiology, Penn State College Medicine, Hershey, Pennsylvania, United States

* To whom correspondence should be addressed. E-mail: clang{at}psu.edu.

The present study determined whether thermal injury increases the expression of the ubiquitin (Ub) E3 ligases referred to as muscle ring finger (MuRF)-1 and muscle atrophy F-box (MAFbx; aka atrogin-1) which are muscle-specific and responsible for the increased protein breakdown observed in other catabolic conditions. After 48 h of burn injury (40% total body surface area full-thickness scald burn), gastrocnemius weight was reduced and this change was associated with an increased mRNA abundance for atrogin-1 and MuRF1 (3.1- to 8-fold, respectively). Similarly, burn increased polyUb mRNA content in the gastrocnemius 2-fold. In contrast, there was no burn-induced atrophy of the soleus nor a significance change in atrogin-1, MuRF1 or polyUb mRNA. Burns also did not alter E3 ligase expression in heart. Four hours after administration of the anabolic agent insulin-like growth factor (IGF)-I to burned rats, the mRNA content of atrogin-1 and polyUb in gastrocnemius had returned to control values, and the elevation in MuRF1 was reduced 50%. In contrast, leucine did not alter E3 ligase expression. In a separate study, in vivo administration of the proteasome inhibitor Velcade prevented burn-induced loss of muscle mass determined at 48 h. Finally, administration of the glucocorticoid receptor antagonist RU486 did not prevent burn-induced atrophy of the gastrocnemius or the associated elevation in atrogin-1, MuRF1 or polyUb. In summary, the acute muscle wasting accompanying thermal injury is associated with a glucocorticoid-independent increase in the expression of several Ub E3 ligases which can be down regulated by IGF-I.




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