Magnetic field-induced Ca intake by mesenchymal stem cells is mediated by intracellular Zn and accompanied by a Zn influx.

Chronic exposure to magnetic fields (MFs) has a diverse range of effects on biological systems but definitive molecular mechanisms of the interaction remain largely unknown. One of the most frequently reported effects of MF exposure is an elevated concentration of intracellular Ca through disputed pathways. Other prominent effects include increased oxidative stress and upregulation of neural markers through EGFR activation in stem cells. Further characterization of cascades triggered by MF exposure is hindered by the phenotype diversity of biological models used in the literature. In an attempt to reveal more mechanistic data in this field, we combined the most commonly used biological model and MF parameters with the most commonly reported effects of MFs. Based on clues from the pathways previously defined as sensitive to MFs (EGFR and Zn-binding enzymes), the roles of different types of channels (voltage gated Ca channels, NMDA receptors, TRP channels) were inquired in the effects of 50 Hz MFs on bone marrow-derived mesenchymal stem cells. We report that, an influx of Zn accompanies MF-induced Ca intake, which is only attenuated by the broad-range inhibitor of TRP channels and store-operated Ca entry (SOCE), 2-Aminoethoxydiphenyl borate (2-APB) among other blockers (memantine, nifedipine, ethosuximide and gabapentin). Interestingly, cation influx completely disappears when intracellular Zn is chelated. Our results rule out voltage gated Ca channels as a gateway to MF-induced Ca intake and suggest Zn-related channels as a new focus in the field.