Electromagnetic Fields for the Regulation of Neural Stem Cells

Figure 2

Potential mechanisms of electromagnetic field regulation on neural stem cells. Ca²⁺ and CREB might be the hinge of effects, because of a lack of excitability of NSCs, and according to the Faraday effects, a possible mechanism could be that the MFs facilitate the exchange of intracellular and extracellular ions through these long-term opened ion channels and upregulate the expression of voltage-gated Ca²⁺ channels (VGCCs) or TRPC1 result in a current and potential difference of NSCs, Ca²⁺ flood into from extracellular matrix or endoplasmic reticulum through the voltage-dependent channel or the force of MF itself; on the one hand, intracellular Ca²⁺ stimulates phosphorylation of transcription factor CREB activating the CREB signaling pathway, pCREB recruits more CBP, and p300 initiates the transcriptional machinery, including histone acetyltransferase. Alternatively, calcium or other ELFEF-activated signals could induce histone modifications and chromatin unravelling, leading to the pCREB binding and the start of transcription. On the other hand, the pCREB is able to bind to the promoter of a series of miRNAs to modulate their expression. In addition, CREB itself as well as the epigenetics mechanisms could affect the expression of BDNF which plays a critical role in the activities of NSCs.