Immune Netw.  2011 Aug;11(4):223-226. 10.4110/in.2011.11.4.223.

IGF-I Exerts an Anti-inflammatory Effect on Skeletal Muscle Cells through Down-regulation of TLR4 Signaling

Affiliations
  • 1Department of Exercise Science, College of Health Science, Ewha Womans University, Seoul 120-750, Korea. jun@ewha.ac.kr

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.

Keyword

Insulin-like growth factor-I; Toll-like receptor-4; Cytokines; Skeletal muscle cells; PI3K/Akt; MAPK

MeSH Terms

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
Cytokines
Insulin-Like Growth Factor I
Intercellular Signaling Peptides and Proteins
Interleukin-6
Toll-Like Receptor 4
Tumor Necrosis Factor-alpha
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