Heme oxygenase-1 protects human periodontal ligament cells against substance P-induced RANKL expression

J Periodontal Res. 2010 Jun;45(3):367-74. doi: 10.1111/j.1600-0765.2009.01247.x. Epub 2010 Mar 9.

Abstract

Background and objective: Although substance P (SP) stimulates bone resorption activity and this is reported to be correlated with the degree of periodontal inflammation, it is unclear how human periodontal ligament cells regulate neuropeptide-induced osteoclastogenesis or the possible involvement of heme oxygenase-1 (HO-1) might be. This study examines how SP affects osteoprotegerin (OPG) and RANKL expression via HO-1.

Material and methods: Using immortalized human periodontal ligament cells, the effects of SP on the expression of HO-1, RANKL and OPG mRNA and proteins were determined by RT-PCR and western blotting, respectively. Various concentrations of SP (10(-7), 10(-8), 10(-9) and 10(-10) m) were added to the medium, and the cells were treated for 0, 0.25, 0.5, 1, 2 and 3 d.

Results: Substance P upregulated RANKL and HO-1 and downregulated OPG mRNA and protein expression in periodontal ligament cells, in a concentration- and time-dependent manner. A HO-1 inducer inhibited both the upregulation of RANKL expression and downregulation of OPG expression by SP in periodontal ligament cells. By contrast, treatment with a HO-1 inhibitor or HO-1 small interferring RNA (siRNA) enhanced SP-stimulated RANKL expression. Inhibitors of ERK and p38 MAP kinases, phosphoinositide 3-kinase and nuclear factor-kappaB blocked the effects of SP on RANKL expression in periodontal ligament cells.

Conclusion: These results suggest that SP stimulates osteoclastic differentiation by increasing the expression of RANKL vs. OPG via the HO-1 pathway in periodontal ligament cells. The HO-1 pathway may be an effective therapeutic target for inhibiting chronic periodontitis involving alveolar bone resorption.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation / drug effects
  • Cell Line
  • Cell Nucleus / chemistry
  • Cytosol / chemistry
  • Dose-Response Relationship, Drug
  • Enzyme Induction
  • Enzyme Inhibitors / pharmacology
  • Heme Oxygenase-1 / antagonists & inhibitors
  • Heme Oxygenase-1 / biosynthesis
  • Heme Oxygenase-1 / pharmacology*
  • Hemin / pharmacology
  • Humans
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • NF-E2-Related Factor 2 / analysis
  • NF-kappa B / antagonists & inhibitors
  • Osteoclasts / drug effects
  • Osteoprotegerin / drug effects
  • Osteoprotegerin / metabolism
  • Periodontal Ligament / cytology*
  • Periodontal Ligament / drug effects
  • Phosphoinositide-3 Kinase Inhibitors
  • Protoporphyrins / pharmacology
  • RANK Ligand / drug effects*
  • RANK Ligand / metabolism
  • RNA, Small Interfering / pharmacology
  • Substance P / administration & dosage
  • Substance P / pharmacology*
  • Time Factors
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

Substances

  • Enzyme Inhibitors
  • NF-E2-Related Factor 2
  • NF-kappa B
  • NFE2L2 protein, human
  • Osteoprotegerin
  • Phosphoinositide-3 Kinase Inhibitors
  • Protoporphyrins
  • RANK Ligand
  • RNA, Small Interfering
  • zinc protoporphyrin
  • Substance P
  • Hemin
  • Heme Oxygenase-1
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases