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
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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“Also, the ability of IL-15 to induce hypertrophy in SkM cells has been demonstrated through the reduction of the rate of protein degradation during cachexia and sarcopenia, highlighting the therapeutic power of this cytokine (Quinn et al., 2002).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Quinn et al., 2002
In the citing paper
“In vitro, IL-15 has an anabolic effect by inducing myosin chain synthesis in myotubes [52], notably in response to TNF-α stimulation [53].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [52]
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Hyödynmaa, J. (2015) · Jyväskylä University Digital Archive (University of Jyväskylä)
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)
- 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
- 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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