Human Periodontal Ligament Cells Secrete Macrophage Colony-Stimulating Factor in Response to Tumor Necrosis Factor-Alpha In Vitro
- Autores: Tussanee Yongchaitrakul, Kanokporn Lertsirirangson, Prasit Pavasant
- Localización: Journal of periodontology, ISSN 0022-3492, Vol. 77, Nº. 6, 2006, págs. 955-962
- Idioma: inglés
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Resumen
Background: Human periodontal ligament (HPDL) cells may support osteoclastogenesis by expressing receptor activator of nuclear factor-kappa B ligand (RANKL) in response to periopathogenic factors and inflammatory cytokines. Because osteoclastogenesis requires the presence of macrophage colony-stimulating factor (M-CSF), we examined whether HPDL cells secrete M-CSF in response to tumor necrosis factor-alpha (TNF-α).
Methods: Cultured HPDL cells were treated with TNF-α in serum-free condition. The expression of M-CSF and RANKL was determined by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Inhibitors and anti-TNF receptor (TNFR) neutralizing antibodies were used for the inhibitory experiments. A migration assay was performed.
Results: TNF-α upregulated M-CSF and RANKL in HPDL cells. The effect on M-CSF expression could be partially blocked by pyrrolidine-dithiocarbamate ammonium salt and LY294002 but not by NS398. Neutralizing antibody to TNFR1 could diminish the effect of TNF-α. In addition, TNF-treated culture medium exhibited chemotactic effect for RAW264.7.
Conclusions: HPDL cells are capable of secreting M-CSF and expressing RANKL in response to TNF-α. The upregulation of M-CSF is possibly one of the mechanisms essential for periodontal tissue destruction in response to inflammatory cytokines. The upregulation is partly through nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3′-kinase and possibly involves TNFR1.
