The role of the calmodulin-dependent pathway in static magnetic field-induced mechanotransduction

Bioelectromagnetics. 2010 May;31(4):255-61. doi: 10.1002/bem.20559.

Abstract

While the effects of static magnetic fields (SMFs) on osteoblastic differentiation are well demonstrated, the mechanotransduction pathways of SMFs are still unclear. The aim of this study was to explore the role of calmodulin in the biophysical effects of SMFs on osteoblastic cells. MG63 cells were exposed to a 0.4 T SMF. The expression of phosphodiesterase RNA in the cytoplasm was tested using real-time polymerase chain reaction. The differentiation of the cells was assessed by detecting changes in alkaline phosphatase activity. The role of calmodulin antagonist W-7 was used to evaluate alterations in osteoblastic proliferation and differentiation after the SMF simulations. Our results showed that SMF exposure increased alkaline phosphatase activity and phosphodiesterase 1C gene expression in MG63 cells. Addition of W-7 significantly inhibited the SMF-induced cellular response. We suggest that one possible mechanism by which SMFs affects osteoblastic maturation is through a calmodulin-dependent mechanotransduction pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calmodulin / antagonists & inhibitors
  • Calmodulin / physiology*
  • Cell Proliferation / drug effects
  • Cell Proliferation / radiation effects
  • Cells, Cultured
  • Cyclic Nucleotide Phosphodiesterases, Type 1 / biosynthesis
  • Electromagnetic Fields*
  • Humans
  • Mechanotransduction, Cellular*
  • Osteoblasts / physiology
  • Osteoblasts / radiation effects*
  • Sulfonamides / pharmacology

Substances

  • Calmodulin
  • Sulfonamides
  • W 7
  • Cyclic Nucleotide Phosphodiesterases, Type 1
  • PDE1C protein, human