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Static, Low-Frequency, and Pulsed Magnetic Fields
bound to the plasma membrane of TPA-differentiated U937 and THP-1 cells increased.
Conversely, the rate of phagocytosis of apoptotic cells increased under SMF exposure,
whereas the number of apoptotic cells bound to the plasma membrane of isolated human
Kupffer cells, RAW 264.7 macrophages, and TPA-differentiated THP-1 and U937 cells
decreased. In nondifferentiated U937 and THP-1 cells, SMF exposure enhanced the
number of cell surface–bound apoptotic cells and latex beads.
Kim et al. (2005) studied the effects of various SMFs (1–10 mT) on the adsorption of
specific recombinant fibronectin (FN) peptide (hFNIII9-10) on the titanium surface in
human osteosarcoma TE-85 cells. The authors found significant increases in cell attachment and proliferation, especially in cells exposed to a field of 1 mT. However, SMFs of
up to 10 mT did not influence FN adsorption on the titanium surface.
Ventura et al. (2005) showed that the exposure of pluripotent mouse embryonic
stem (ES) cells to an ELF-EMF (50 Hz, 0.8 mT) triggered the expression of GATA-4
and Nkx-2.5, acting as cardiac lineage-promoting genes in different animal species, as
well as humans. The ELF-EMF also enhanced prodynorphin gene expression and the
synthesis and secretion of dynorphin B, an endorphin playing a major role in cardiogenesis. These effects occurred at the transcriptional level and ultimately resulted in
a remarkable increase in the yield of ES-derived cardiomyocytes. These results demonstrate the potential use of ELF-EMFs in modifying the gene program of cardiac
differentiation in ES cells without the aid of gene transfer technologies and suggest
that this development may pave the way for novel approaches in tissue engineering
and cell therapy.
Mannerling et al. (2010) reported the influence of ELF-EMFs (50 Hz, 0.025–0.10 mT,
for 1 hour) on different cellular parameters in human leukaemia cells (K562). The positive control heat treatment (42°C, for 1 hour) did not affect either cell proliferation or
superoxide radical anion production but caused accumulation of cells in the G 2 phase
and increased the stress protein HSP70. The EMF exposure (0.10 mT, for one hour)
did not affect either cell cycle kinetics or proliferation. Both vertical and horizontal
EMF exposures for one hour caused significantly and transiently increased HSP70 levels (more than twofold) at several flux densities, compared with the sham controls and
the heat treatment. This exposure also increased (by 30%–40%) the levels of the superoxide radical anion, which was comparable to the positive control phorbol myristate
acetate. Addition of free radical scavengers (melatonin or 1,10-phenantroline) inhibited the EMF-induced increase in HSP70. In conclusion, an early response to EMF in
K562 cells seems to be the presence of an increased amount of oxygen radicals, leading
to HSP70 induction. Furthermore, the results suggest that the effective flux density
threshold is ≤0.025 mT, and also that it is the EMF and not the induced electric field
that is the active field.
Jansen et al. (2010) investigated the effect of a PEMF (15 Hz, 100 μT, 5-millisecond
bursts with 5-microsecond pulses) on human bone marrow–derived stromal cell
(BMSC) metabolism and investigated, specifically, whether the PEMF can stimulate the
osteogenic differentiation of BMSC. The authors suggest that PEMF exposure enhances
mineralization and induces differentiation at the expense of proliferation. The osteogenic stimulus of PEMF was confirmed by the upregulation of several osteogenic marker
genes in the PEMF-treated group, which preceded the deposition of mineral itself.