Question: 

The cell membrane is often considered as the main target for magnetic fields (MFs), and it has been suggested that even a small change in transmembrane voltage could trigger a significant modulation of cell function. In the present study it was hypothesized that MFs enhance cardiomyogenesis from Flk-1⁺ cardiac progenitor cells.

Methods and results: 

We and others have previously demonstrated that cardiovascular cell types can be differentiated from Flk-1⁺ progenitor cells isolated from embryonic stem (ES) cells. In Flk-1⁺ cells isolated from Embryoid Bodies (EBs) static MFs (1 mT) elevated both cellular calcium ([Ca²⁺]_c) and reactive oxygen species (ROS), increased expression of the cardiogenic transcription factors Nkx-2.5 and GATA-4 as well as the cardiac genes MLC2a, MLC2v, a-MHC and b-MHC. This effect was due to increased Ca²⁺ influx, since extracellular Ca²⁺ chelation abrogated ROS production and MF-induced cardiomyogenesis. Furthermore absence of extracellular calcium impaired sarcomere structure formation. Neither the phospholipase C inhibitor U73122 nor thapsigargin inhibited static MF-induced increase in [Ca²⁺]_c excluding involvement of intracellular calcium stores. ROS were generated through NAD(P)H oxidase, since NOX-4 but not NOX-1 and NOX-2 mRNA expression was upregulated upon MF exposure, and the NAD(P)H oxidase inhibitor diphenylen iodonium (DPI) totally abolished the observed effect. The data of the present study demonstrate that Ca²⁺ is involved in ROS formation and initiation of ES cell cardiomyogenesis.

Conclusion: 

The ability of static MFs to enhance cardiomyocyte differentiation of ES cells allows high throughput generation of cardiomyocytes without pharmacological or genetic modification.