Key result
Exposure to a 0.4 T static magnetic field increased alkaline phosphatase activity and phosphodiesterase 1C gene expression in MG63 cells, an effect significantly inhibited by calmodulin antagonist W-7.
Static magnetic fields may affect osteoblastic maturation through a calmodulin-dependent mechanotransduction pathway.
In vitro findings implicate calmodulin in osteoblast responses to static fields; leaves open translation to bone healing or clinical use.
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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Yang et al. (2009) studied this question. 0.4 T static magnetic field (SMF) was evaluated on Alkaline phosphatase activity and phosphodiesterase 1C gene expression. Exposure to a 0.4 T static magnetic field increased alkaline phosphatase activity and phosphodiesterase 1C gene expression in MG63 cells, an effect significantly inhibited by calmodulin antagonist W-7.
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