期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 98, 期 3, 页码 911-917出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.01026.2004
关键词
suppressor of cytokine signaling; signal transducer activator of transcription; insulin-like growth factor I; 70-kDa ribosomal S6 kinase
资金
- NIAMS NIH HHS [AR-45594] Funding Source: Medline
Chronic, low-level elevation of circulating interleukin (IL)-6 is observed in disease states as well as in many outwardly healthy elderly individuals. Increased plasma IL-6 is also observed after 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 present study, we used a rodent local infusion model to deliver modest levels of IL-6, comparable to that present after 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 STAT5 ( - 33%), whereas that of STAT3 was increased approximately twofold. 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 downregulation 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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