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Cited by 226Muscle Physiology and DisordersMuscle metabolism and nutritionNutrition and Health in Aging

The DOI matches its Crossref record; 53 of the 54 references it cites were found in a registry or an index.

Overexpression of Interleukin-15 Induces Skeletal Muscle Hypertrophy in Vitro: Implications for Treatment of Muscle Wasting Disorders

Quinn, LeBris S., Anderson, Barbara G., Drivdahl, Rolf H., Alvarez, Belén, Argilés, Josep M.·2002·Experimental Cell Research
DOI 10.1006/excr.2002.5624
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Abstract

Interleukin-15 (IL-15) is a novel anabolic factor for skeletal muscle which inhibits muscle wasting associated with cancer (cachexia) in a rat model. To develop a cell culture system in which the mechanism of the anabolic action of IL-15 on skeletal muscle could be examined, the mouse C2 skeletal myogenic cell line was transduced with a retroviral expression vector for IL-15 and compared to sister cells transduced with a control vector. Overexpression of IL-15 induced fivefold higher levels of sarcomeric myosin heavy chain and alpha-actin accumulation in differentiated myotubes. Secreted factors from IL-15-overexpressing myogenic cells, but not from control cells, induced increased myofibrillar protein accumulation in cocultured control myotubes. IL-15 overexpression induced a hypertrophic myotube morphology similar to that described for cultured myotubes which overexpressed the well-characterized anabolic factor insulin-like growth factor-I (IGF-I). However, in contrast to IGF-I, the hypertrophic action of IL-15 on skeletal myogenic cells did not involve stimulation of skeletal myoblast proliferation or differentiation. IL-15 induced myotube hypertrophy at both low and high IGF-I concentrations. Furthermore, in contrast to IGF-I, which stimulated only protein synthesis under these culture conditions, IL-15 both stimulated protein synthesis and inhibited protein degradation in cultured skeletal myotubes. These findings indicate that IL-15 action on skeletal myogenic cells is distinct from that of IGF-I. Due to the ability of IGF-I to stimulate cell division and its association with several forms of cancer, controversy exists concerning the advisability of treating cachexia or age-associated muscle wasting with IGF-I. Administration of IL-15 or modulation of the IL-15 signaling pathway may represent an alternative strategy for maintaining skeletal muscle mass under these conditions.

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Research works printed but not linked: 2

  1. Damon, 1998, Retrovirally mediated overexpression of insulin-like growth factor binding protein 4: Evidence that insulin-like growth factor in required for skeletal muscle differentiation, J. Cell. Physiol., 177, 47
  2. Argilés, 1997, Cancer cachexia: A key role for TNF?, Int. J. Oncol., 10, 565

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Metadata

Authors
Quinn, L. S., Anderson, B. G., Drivdahl, R. H., Alvarez, B., & Argilés, J. M.
Affiliations
  • University of Washington (US)
  • Universitat de Barcelona (ES)
ORCID
Argilés, Josep M.
Venue
Experimental Cell Research
Publisher
Elsevier BV
Published
2002-10
Volume
280
Issue
1
Pages
55-63
ISSN
0014-4827 (ISSN-L)
DOI
10.1006/excr.2002.5624
OpenAlex
W1989771979
Cited by
226
References
54
Citations by year
2026: 9 · 2025: 3 · 2024: 10 · 2023: 13 · 2022: 10 · 2021: 8 · 2020: 8 · 2019: 10 · 2018: 14 · 2017: 7 · 2016: 8 · 2015: 15 · 2014: 8 · 2013: 19 · 2012: 12
FWCI
2.32
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Cell Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
  • Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
Keywords
IL-15, skeletal muscle hypertrophy, muscle atrophy, cachexia, cancer cachexia, insulin-like growth factor I, myotube differentiation, myosin heavy chain, alpha-actin, protein synthesis, protein degradation, retroviral gene transfer
MeSH terms
Actins, Animals, Cachexia, Cell Line, Cells, Cultured, DNA, Genetic Vectors, Hypertrophy, Muscular Diseases, Retroviridae, Sarcomeres, Somatomedins, Transduction, Genetic, Muscle, Skeletal, Coculture Techniques, Myosin Heavy Chains, Interleukin-15, Mice

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