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1 Cell Molec Physiology, Penn State College Medicine, Hershey, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: clang{at}psu.edu.
Various atrophic stimuli increase two muscle-specific E3 ligases - muscle ring finger (MuRF)-1 and atrogin-1, and knockout mice for these atrogenes display resistance to denervation-induced atrophy. The present study determined whether increased atrogin-1 and MuRF1 mRNA is mediated by over-production of endogenous glucocorticoids or inflammatory cytokines in adult rats and whether atrogene expression can be down-regulated by anabolic agents such as insulin-like growth factor (IGF)-I and the nutrient signaling amino acid leucine. Both atrogin-1 and MuRF1 mRNA in gastrocnemius was up-regulated dose- and time-dependently by endotoxin. Additionally, peritonitis produced by cecal ligation and puncture increased atrogin-1 and MuRF1 mRNA in gastrocnemius (but not soleus or heart) by 8 h which was sustained for 72 and 24 h, respectively. While the sepsis-induced increase in atrogin-1 expression was completely prevented by IGF-I, the increased MuRF1 was not altered. In contrast to the IGF-I effect, the sepsis-induced increased mRNA of both atrogenes was unresponsive to either acute or chronic administration of leucine. While exogenous infusion of TNF
increased atrogin-1 and MuRF1 in gastrocnemius, pretreatment of septic rats with the TNF antagonist TNF binding protein did not prevent increased expression of either atrogene. Similarly, while dexamethasone increased atrogene expression, pretreatment with the glucocorticoid receptor antagonist RU486 failed to ameliorate the sepsis-induced increase in atrogin-1 and MuRF1. Thus, under in vivo conditions in mature adult rats, the sepsis-induced increase in muscle atrogin-1 and MuRF1 mRNA appears both glucocorticoid- and TNF-independent, and is unresponsive to leucine.
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