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1 Department of Physiology & Biophysics, University of California Irvine, Irvine, CA, USA
2 Department of Pediatrics, University of California Irvine, Irvine, CA, USA
* To whom correspondence should be addressed. E-mail: gradams{at}uci.edu.
Chronic, low level, elevation of circulating interleukin-6 (IL-6) is observed in disease states as well as in many outwardly healthy elderly individuals. Increased plasma IL-6 is also observed following intense, prolonged exercise. In the context of skeletal muscle, IL-6 has variously been reported to regulate carbohydrate and lipid metabolism, increase satellite cell proliferation or cause muscle wasting. In the current study we used a rodent local infusion model to deliver modest levels of IL-6, comparable to that present following exercise or with chronic low level inflammation in the elderly, directly into a single target muscle in vivo. The aim of this study was to examine the direct effects of IL-6 on skeletal muscle in the absence of systemic changes in this cytokine. Data included cellular and molecular markers of cytokine and growth factor signaling (phosphorylation and mRNA content) as well as measurements to detect muscle atrophy. IL-6 infusion resulted in muscle atrophy characterized by a preferential loss of myofibrillar protein (-17%). IL-6 induced a decrease in the phosphorylation of ribosomal S6 kinase (-60%) and Signal Transducer Activator of Transcription (STAT)-5 (-33%) while that of STAT3 was increased ~2 fold. The changes seen in the IL-6 infused muscles suggest alterations in the balance of growth factor related signaling in favor of a more catabolic profile. This suggests that down regulation of growth factor mediated intracellular signaling may be a mechanism contributing to the development of muscle atrophy induced by elevated IL-6.
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