Additionally, the effect of insulin-like growth factor I (IGF-I ) and of signal transduction inhibitors (involving the extracellular signal-regulated kinase 1/2, phosphatidylinositol 3 -kinase, and p38 mitogen-activated protein kinase) plus/without electromagnetic field exposure were evaluated to get insight into cellular differentiation mechanisms. Cells were examined after 14 and 21 days culture period.
|Setup||coil consisting of primary and secondary windings wound round a polyvinyl chloride container with an inner diameter of 34.5 cm and an outer diameter of 37 cm; primary coil consisting of 150 turns of 2.12 mm enameled wire; second coil separated into two pieces, each made of three layers with 33 turns of 2.12 mm enameled wire; coil placed inside a plastic container; cells inside a CO2 incubator in the center of the coil|
|magnetic flux density||3 mT||-||-||-||-|
Exposure to the extremely low frequency field increased significantly the intracellular collagen.
Treatment with an inhibitor of extracellular signal-regulated kinase 1/2 reduced the collagen content in all of the cells examined (control group, group treated with insulin-like growth factor I or extremely low frequency field exposure alone or in combination). However, the inhibitor of extracellular signal-regulated kinase 1/2 did not prevent the intracellular collagen increase caused by the exposure, and insulin-like growth factor I alone. The phosphatidylinositol 3-kinase pathway inhibitor induced an acceleated increase in intracellular collagen after exposure. However, the increase in collagen observed by insulin-like growth factor I addition was suppressed. The p38 mitogen-activated protein kinase inhibitor suppressed the increase in the collagen induced by the exposure, whereas insulin-like growth factor I addition increased the collagen in the presence of the inhibitor.
These data suggest that collagen synthesis induced by the extremely low frequency exposure was carried out by the participation of p38 MAPK pathway, and that phosphatidylinositol 3-kinase pathway may have the role to suppress the collagen synthesis, and that the suppression of the phosphatidylinositol 3-kinase pathway may allow the acceleration of the exposure induced collagen synthesis.