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.

Original languageEnglish
Pages (from-to)255-261
Number of pages7
JournalBioelectromagnetics
Volume31
Issue number4
DOIs
Publication statusPublished - May 2010

Fingerprint

Magnetic Fields
Calmodulin
Alkaline Phosphatase
Phosphodiesterase I
Phosphoric Diester Hydrolases
Real-Time Polymerase Chain Reaction
Cell Differentiation
Cytoplasm
RNA
Gene Expression

Keywords

  • Calmodulin
  • Mechanobiology
  • Osteoblast
  • Phosphodiesterase
  • Static magnetic field

ASJC Scopus subject areas

  • Biophysics
  • Radiology Nuclear Medicine and imaging
  • Physiology

Cite this

The role of the calmodulin-dependent pathway in static magnetic field-induced mechanotransduction. / Yang, Jen Chang; Lee, Sheng Yang; Chen, Chi An; Lin, Che Tong; Chen, Chang Chih; Huang, Haw Ming.

In: Bioelectromagnetics, Vol. 31, No. 4, 05.2010, p. 255-261.

Research output: Contribution to journalArticle

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AU - Lee, Sheng Yang

AU - Chen, Chi An

AU - Lin, Che Tong

AU - Chen, Chang Chih

AU - Huang, Haw Ming

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N2 - 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.

AB - 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.

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