Inhibitory effect of cantharidin on osteoclast differentiation and bone resorption

Arch Pharm Res. 2010 Mar;33(3):457-62. doi: 10.1007/s12272-010-0316-0. Epub 2010 Mar 30.

Abstract

Regulation of receptor activator of nuclear factor kappaB-ligand (RANKL)-induced osteoclast differentiation is of current interest in the development of antiresorptive agents. We identified the inhibitory effects of cantharidin on RANKL-induced differentiation and bone resorptive activities of osteoclasts in macrophage-like RAW264.7 cells. Interestingly, cantharidin significantly inhibited RANKL-induced ERK/MAP kinase activation and protein phosphatase 2A (PP2A) activity. In addition, cantharidin significantly inhibited RANKL-induced mRNA expression of transcription factors and osteoclast-specific genes (especially Fra-2 and cathepsin K, respectively). Although further studies might be required to elucidate the precise mechanism of cantharidin's action on osteoclast differentiation and bone resorptive activities, our results suggested that cantharidin-mediated inactivation of PP2A could prevent RANKLinduced activation of ERK/MAP kinase and transcription factors such as AP-1 and NFATc1, with subsequent inhibition of osteoclast-specific gene expression required for efficient osteoclast differentiation and bone resorption.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bone Density Conservation Agents / pharmacology*
  • Bone Resorption / genetics
  • Bone Resorption / metabolism
  • Bone Resorption / pathology
  • Bone Resorption / prevention & control*
  • Cantharidin / pharmacology*
  • Cathepsin K / metabolism
  • Cell Differentiation / drug effects*
  • Cell Differentiation / genetics
  • Cell Line
  • Dose-Response Relationship, Drug
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Fos-Related Antigen-2 / genetics
  • Gene Expression Regulation / drug effects
  • Mice
  • NFATC Transcription Factors / genetics
  • Osteoclasts / drug effects*
  • Osteoclasts / metabolism
  • Osteoclasts / pathology
  • Phosphorylation
  • Protein Phosphatase 2 / antagonists & inhibitors
  • Protein Phosphatase 2 / metabolism
  • RANK Ligand / metabolism
  • RNA, Messenger / metabolism
  • Transcription Factor AP-1 / genetics

Substances

  • Bone Density Conservation Agents
  • Enzyme Inhibitors
  • Fos-Related Antigen-2
  • NFATC Transcription Factors
  • Nfatc1 protein, mouse
  • RANK Ligand
  • RNA, Messenger
  • Transcription Factor AP-1
  • Extracellular Signal-Regulated MAP Kinases
  • Protein Phosphatase 2
  • Cathepsin K
  • Ctsk protein, mouse
  • Cantharidin