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gangliosides, time-dependent regulation of IL-6 signaling by glycosphingolipids, and
the fate of embryonic cells. Furthermore, Wang et al. (2010) reported that SMF exposure
elicited qualitatively similar responses as ZM241385, a PD drug candidate.
Khodarahmi, Mobasheri, and Firouzi (2010) examined the effect of a homogeneous
SMF of 2.1 T on viability and morphology of rat astrocytes; but the study showed that
the SMF exposure for 72 hours did not significantly affect the viability and morphological properties. Hirai et al. (2006) screened genes responsive to brief exposure to an SMF
(100 mT, for 15 min) in cultured rat hippocampal neurons. The authors cloned and identified Ntan1 (amidohydrolase for N-terminal asparagine) as an SMF-responsive gene in
rat brain. Ntan1 is an essential component of a protein degradation signal, which is a
destabilizing N-terminal residue of a protein, in the N-end rule. Northern blot analysis
showed that Ntan1 mRNA level was increased by about threefold 3 hours after exposure. The SMF also increased the transcriptional activity of Ntan1 promoter. The SMF
induced degradation of microtubule-associated protein 2 (MAP2) without affecting
cell morphology and viability, which was prevented by a selective inhibitor of 26S proteasome in hippocampal neurons. Overexpression of Ntan1 using recombinant Ntan1
adenovirus vector resulted in a marked decrease in MAP2 expression in hippocampal
neurons. The results suggest that brief exposures to SMF leads to the induction of Ntan1
responsible for MAP2 degradation through the ubiquitin–proteasome pathway in rat
hippocampal neurons.
Yang et al. (2010) explored the role of calmodulin in the effects of an SMF (400 mT)
on osteoblastic MG63 cells. The role of calmodulin antagonist W-7 was used to evaluate
alterations in osteoblastic proliferation and differentiation after exposure. The results
showed that SMF increased ALP activity and phosphodiesterase 1C gene expression in
MG63 cells. Addition of W-7 significantly inhibited the SMF-induced cellular response.
The authors suggested that one possible mechanism by which SMF affects osteoblastic
maturation is a calmodulin-dependent mechanotransduction pathway.
Sakurai, Terashima, and Miyakoshi (2008) investigated whether exposure to an
inhomogeneous strong SMF of 10 T affects prostaglandin E 2 (PGE 2 ) secretion from
a mouse osteoblastic cell line, MC3T3-E1. The authors also investigated the PGE 2 ­
synthesizing enzyme, COX-2, and translocation of NF-κB, which is involved in the
induction of COX-2 expression. An inhomogeneous SMF exposure was performed at
the 10 T-exposure position, at which the magnetic flux density was found to be the
highest, and at the 6 T-exposure position, at which the magnetic gradient was found
to be the highest (41.7 T/m). The secretion of PGE 2 was not affected by exposure at
the 10 T-exposure position compared with sham exposure, but it was enhanced at the
6 T-exposure position (by about 1.5-fold). Similarly, COX-2 expression and NF-κB
translocation were not enhanced at the 10 T-exposure position, but they increased at
the 6 T-exposure position (by about twofold and two- to threefold, respectively). These
findings suggested that exposure to a high magnetic gradient induced the secretion of
PGE 2 and the expression of the COX-2 protein, which was mediated through increased
translocation of NF-κB.
The same research group (Sakurai, Terashima, and Miyakoshi 2009) further evaluated the effects of a strong SMF (10 T) on glucose-metabolic pathways. Hamster-derived
insulin-secreting cells (HIT-T15) were cultured under exposure to sham and SMF