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

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