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IL-6-induced skeletal muscle atrophy

Haddad, F ; Zaldivar, F ; Cooper, D. M ; Adams, G. R

Journal of applied physiology (1985), 2005-03, Vol.98 (3), p.911-917 [Periódico revisado por pares]

Bethesda, MD: Am Physiological Soc

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  • Título:
    IL-6-induced skeletal muscle atrophy
  • Autor: Haddad, F ; Zaldivar, F ; Cooper, D. M ; Adams, G. R
  • Assuntos: Animals ; Biological and medical sciences ; Cytokines ; Exercise ; Female ; Fundamental and applied biological sciences. Psychology ; Interleukin-6 - administration & dosage ; Interleukin-6 - adverse effects ; Muscle Proteins - metabolism ; Muscular Atrophy - chemically induced ; Muscular Atrophy - physiopathology ; Muscular system ; Rats ; Rats, Sprague-Dawley ; Signal Transduction - drug effects ; Striated muscle. Tendons ; Vertebrates: osteoarticular system, musculoskeletal system
  • É parte de: Journal of applied physiology (1985), 2005-03, Vol.98 (3), p.911-917
  • Descrição: Departments of 1 Physiology and Biophysics and 2 Pediatrics, University of California, Irvine, California Submitted 16 September 2004 ; accepted in final form 4 November 2004 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. suppressor of cytokine signaling; signal transducer activator of transcription; insulin-like growth factor I; 70-kDa ribosomal S6 kinase Address for reprint requests and other correspondence: G. R. Adams, Associate Researcher, Dept. of Physiology & Biophysics, Univ. of California, Irvine, Medical Sciences 1, Rm. D335, Irvine, CA 92697-4560 (E-mail: GRAdams{at}uci.edu )
  • Editor: Bethesda, MD: Am Physiological Soc
  • Idioma: Inglês
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