Enhanced secretion of prostaglandin E2 from osteoblasts by exposure to a strong static magnetic field
Article first published online: 28 DEC 2007
Copyright © 2007 Wiley-Liss, Inc.
Volume 29, Issue 4, pages 277–283, May 2008
How to Cite
Sakurai, T., Terashima, S. and Miyakoshi, J. (2008), Enhanced secretion of prostaglandin E2 from osteoblasts by exposure to a strong static magnetic field. Bioelectromagnetics, 29: 277–283. doi: 10.1002/bem.20392
- Issue published online: 4 APR 2008
- Article first published online: 28 DEC 2007
- Manuscript Revised: 7 OCT 2007
- Manuscript Received: 18 APR 2007
- static magnetic field;
- magnetic field gradient;
- cyclooxygenase 2;
- transcription factor nuclear factor kappa B
Exposure to static magnetic fields (SMFs) has been reported to promote osteoblast differentiation in vitro, and increase bone formation in vivo and in clinical studies. Prostaglandins respond early to exogenous mechanical loading, and play an important role in bone formation. In this study, we investigated whether exposure to a strong SMF affects prostaglandin E2 (PGE2) secretion from a mouse osteoblastic cell line, MC3T3-E1. We also investigated the PGE2-synthesizing enzyme, cyclooxygenase 2 (Cox-2), and translocation of the transcription factor nuclear factor kappa B (NF-κB), which is involved in the induction of Cox-2 expression. In the SMF exposures, experiments were performed at the 10 T-exposure position, at which the magnetic flux density was highest, and at the 6 T-exposure position, at which the magnetic field gradient was highest (41.7 T/m). PGE2 secretion was not affected by exposure at the 10 T-exposure position compared to sham-exposure, but was enhanced at the 6 T-exposure position (about 1.5-fold). Similarly, Cox-2 expression and NF-κB translocation were not enhanced at the 10 T-exposure position, but increased at the 6 T-exposure position (about twofold, two- to threefold, respectively). These findings suggested that exposure to a high magnetic field gradient induced secretion of PGE2 and expression of the Cox-2 protein, which was mediated through increased translocation of NF-κB. Bioelectromagnetics 29:277–283, 2008. © 2007 Wiley-Liss, Inc.