IGF-I Exerts an Anti-inflammatory Effect on Skeletal Muscle Cells through Down-regulation of TLR4 Signaling.
- Author:
Won Jun LEE
1
Author Information
- Publication Type:Brief Communication
- Keywords: Insulin-like growth factor-I; Toll-like receptor-4; Cytokines; Skeletal muscle cells; PI3K/Akt; MAPK
- MeSH: Cytokines; Down-Regulation; Insulin-Like Growth Factor I; Intercellular Signaling Peptides and Proteins; Interleukin-6; Muscle, Skeletal; Toll-Like Receptor 4; Tumor Necrosis Factor-alpha
- From:Immune Network 2011;11(4):223-226
- CountryRepublic of Korea
- Language:English
- Abstract: Although exercise-induced growth factors such as Insulin-like growth factor-I (IGF-I) are known to affect various aspects of physiology in skeletal muscle cells, the molecular mechanism by which IGF-I modulates anti-inflammatory effects in these cells is presently unknown. Here, we showed that IGF-I stimulation suppresses the expression of toll-like receptor 4 (TLR4), a key innate immune receptor. A pharmacological inhibitor study further showed that PI3K/Akt signaling pathway is required for IGF-I-mediated negative regulation of TLR4 expression. Furthermore, IGF-I treatment reduced the expression of various NF-kappaB-target genes such as TNF-alpha and IL-6. Taken together, these findings indicate that the anti-inflammatory effect of exercise may be due, at least in part, to IGF-I-induced suppression of TLR4 and subsequent downregulation of the TLR4-dependent inflammatory signaling pathway.
