All experiments are performed at the

All experiments are performed at the same conditions of EMF intensity, frequency, chronical exposure, and temperature. In Table 1, we report the effects of the ELF-EMF exposure on MCP-1 expression in different cell lines.
In HaCaT cells, using RT-PCR we have evidenced a decrease in MCP-1 expression from 4 to 72h in EMF-exposed cox inhibitor with respect to non-exposed cells. This decrease was confirmed by additional Real Time PCR (basal exposed 0.9±0.02 vs. basal non-exposed 1.6±0.05). Also the ELISA immunoassay, performed to evaluate the release of MCP-1, confirmed the expression results. Since it is well accepted that an excessive or prolonged inflammatory response may interfere with wound healing and cause reduction of the inflammatory chemokines by ELF-EMF exposure, represents an interesting and new therapeutic approach in delayed healing.
In SH-SY5Y cell cultures exposed to ELF-EMF, genes involved in the stress response, cell growth and differentiation or protein metabolism have been reported to be generally down-regulated. Genes involved in Ca2+ metabolism, the PI3-kinase pathway are up-regulated. Likewise, key mediators of the inflammatory response appear susceptible to swift modulation, in SH-SY5Y.
MCP-1 is involved in the neuroinflammatory processes associated with diseases characterized by neuronal degeneration. To characterize the impact of ELF-EMF on early ongoing cellular processes, MCP-1 gene expression in SH-SY5Y, was evaluated in the presence and absence of ELF-EMF exposure by RT-PCR. After 24h of ELF-EMF exposure MCP-1 expression was not significantly affected. Albeit our results on MCP-1 expression, despite differences in experimental conditions, are in line with several other ELF-EMF exposure results, while they are not in accord with a study reporting that ELF-EMF promotes cellular neurodifferentiation, as exemplified by neurite extension and number (Falone et al., 2007). In conclusion, our results showed that ELF-EMF exposure is well tolerated and has no relevant impact on MCP-1 gene expression.
The role of MCP-1 in human disease has been demonstrated by immunohistochemical studies in fact the adhesion of cells to the endothelium was induced by expression of adhesion molecules and chemotactic proteins, such as MCP-1. We have analyzed the effects of EMF on the expression of MCP-1 also in THP-1 cells. Since in THP-1 exposed to ELF-EMF no increase in basal levels of MCP-1 was observed, cells were treated or not with LPS and exposed to 50Hz, 1mT EMF for 24hr. Our data indicate that the presence of 10μg/ml of LPS leads to an cox inhibitor increase in expression of MCP-1 in both THP-1 cells non exposed or exposed to EMF. Thus, we hypothesized that MCP-1 mediated THP-1 migration is not affected by EMF exposure, and consequently the exposure to the fields is not a risk factor in diseases in which microglial migration plays a crucial role, such as atherosclerosis, multiple sclerosis and other neuroinflammatory diseases.

Conclusions
The results of in vivo and in vitro studies suggest that EMF may modulate the expression of some inflammatory molecules. The understanding of the influences of EMF on transcriptional events will lead to a better understanding of their mechanisms and to therapeutic interventions for diseases in which these inflammatory molecules play a key role. In spite of the fact that the mechanisms of action of EMF are still under investigation, some authors have supposed that exposure to ELF-EMF affects cell function through mechanical action on both intracellular and membrane proteins, which includes ion channels, membrane receptors and enzymes. All studies agree that the effect of the sinusoidal ELF-EMF varies in relation to cell type and other parameters, such as frequency, flux density and time exposure.
Our data confirm the cell-type dependent effects; in fact we observed increase, decrease or no effect on the MCP-1 expression in different cell lines grown under the same conditions (sinusoidal 50Hz, 1mT, 37°C, 5% CO2).