Magnetic fields promote a pro-survival non-capacitative Ca[super]2+ entry via phospholipase C signaling

The ability of magnetic fields (MFs) to promote/increase Ca[super]2+ influx into cells is widely recognized, but the underlying mechanisms remain obscure. Here we analyze how static MFs of 6 mT modulates thapsigargin-induced Ca[super]2+ movements in non-excitable U937 monocytes, and how this relates to the anti-apoptotic effect of MFs. Magnetic fields do not affect thapsigargin-induced Ca[super]2+ mobilization from endoplasmic reticulum, but significantly increase the resulting Ca[super]2+ influx; this increase requires intracellular signal transduction actors including G protein, phospholipase C, diacylglycerol lipase and nitric oxide synthase, and behaves as a non-capacitative Ca[super]2+ entry (NCCE), a type of influx with an inherent signaling function, rather than a capacitative Ca[super]2+ entry (CCE). All treatments abrogating the extra Ca[super]2+ influx also abrogate the anti-apoptotic effect of MFs, demonstrating that MF-induced NCCE elicits an anti-apoptotic survival pathway.