Stromal cell-derived factor-1/CXCR4 promotes IL-6 production in human synovial fibroblasts

J Cell Biochem. 2011 Apr;112(4):1219-27. doi: 10.1002/jcb.23043.

Abstract

The production of chemokine stromal cell-derived factor (SDF)-1 is significantly higher in synovial fluid of patients with osteoarthritis (OA). IL-6 is a multifunctional cytokine that plays a central role in both OA and rheumatoid arthritis. However, the effects of SDF-1α on human synovial fibroblasts are largely unknown. In this study, we investigated the intracellular signaling pathway involved in SDF-1α-induced IL-6 production in human synovial fibroblast cells. SDF-1α caused concentration- and time-dependent increases in IL-6 production. SDF-1α also increased the mRNA and surface expression of CXCR4 receptor in human synovial fibroblasts. CXCR4-neutralizing antibody, CXCR4-specific inhibitor (AMD3100), or small interfering RNA against CXCR4 inhibited the SDF-1α-induced increase of IL-6 expression. The transcriptional regulation of IL-6 by SDF-1α was mediated by phosphorylation of phosphatidylinositol 3-kinase (PI3K)/Akt and activation of the activator protein (AP)-1 component of c-Jun. The binding of c-Jun to the AP-1 element on the IL-6 promoter and the increase in AP-1 luciferase activity was enhanced by SDF-1α. Co-transfection with CXCR4, PI3K, Akt, and c-Jun mutants or siRNA inhibited the potentiating action of SDF-1α on AP-1 promoter activity. Taken together, our results suggest that SDF-1α-increased IL-6 production in human synovial fibroblasts via the CXCR4 receptor, PI3K, Akt, c-Jun, and AP-1 signaling pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Benzylamines
  • Blotting, Western
  • Cells, Cultured
  • Chemokine CXCL12 / metabolism
  • Chemokine CXCL12 / pharmacology*
  • Cyclams
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Heterocyclic Compounds / pharmacology
  • Humans
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism*
  • JNK Mitogen-Activated Protein Kinases / genetics
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Osteoarthritis / genetics
  • Osteoarthritis / metabolism
  • Osteoarthritis / pathology
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Binding
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference
  • Receptors, CXCR4 / antagonists & inhibitors
  • Receptors, CXCR4 / genetics
  • Receptors, CXCR4 / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Synovial Membrane / metabolism
  • Synovial Membrane / pathology
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism

Substances

  • Benzylamines
  • Chemokine CXCL12
  • Cyclams
  • Heterocyclic Compounds
  • Interleukin-6
  • Receptors, CXCR4
  • Transcription Factor AP-1
  • Proto-Oncogene Proteins c-akt
  • JNK Mitogen-Activated Protein Kinases
  • plerixafor