The JAK2-Akt-glycogen synthase kinase-3 beta signaling pathway is involved in toll-like receptor 2-induced monocyte chemoattractant protein-1 regulation
- The JAK2-Akt-glycogen synthase kinase-3 beta signaling pathway is involved in toll-like receptor 2-induced monocyte chemoattractant protein-1 regulation
- 백석환; 박대원; 이형경; 정태활[정태활]; 김진식[김진식]; 배외식[배외식]; 진병로
- FOAM CELL-FORMATION; INFLAMMATORY HEPATOCELLULAR TUMORS; CARDIOVASCULAR-DISEASE; SOMATIC DELETIONS; EXPRESSION; ATHEROSCLEROSIS; ACTIVATION; TOLL-LIKE-RECEPTOR-2; CHEMOKINES; MCP-1
- Issue Date
- SPANDIDOS PUBL LTD
- MOLECULAR MEDICINE REPORTS, v.5, no.4, pp.1063 - 1067
- Monocyte chemoattractant protein-1 (MCP-1) is an essential cytokine for the migration of monocytes into vessels, and is also involved in the pathogenesis of atherosclerosis. In this study, we investigated the importance of janus kinase 2 (JAK2) and the function of the Akt and glycogen synthase kinase-3 beta (GSK3 beta) pathway in toll-like receptor (TLR2)-mediated MCP-1 expression. The TLR2 agonist, Pam(3)CSK(4), induced MCP-1 expression in the Raw264.7 cell line. The induction of MCP-1 was seen in the bone marrow-derived macrophages of wild-type mice but not in TLR2 knockout mice. The TLR2-mediated MCP-1 induction was myeloid differentiation primary response gene 88 (MyD88)-independent. By contrast, the inactivation of JAK2 attenuated TLR2-mediated MCP-1 expression. The JAK inhibitor suppressed the phosphorylation of GSK3 beta as well as Akt by Pam(3)CSK(4) stimulation. While the inactivation of Akt by LY294002 suppressed TLR2-mediated MCP-1 induction, the inactivation of GSK3 beta by LiCl potentiated TLR2-mediated MCP-1 induction. Furthermore, Akt inhibitor suppressed TLR2-mediated phosphorylation of GSK3 beta. Taken together, these :results suggest that a MyD88-independent pathway exists in TLR2 signaling; the JAK2-Akt-GSK3 beta pathway is a novel MyD88-independent pathway for MCP-1 induction.
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