Int J Biochem Cell Biol 2011 Mar 21;43(3):393-400. Epub 2010 Nov 21.
Dipartimento di Biologia, Universita' degli Studi di Roma Tor Vergata, Via della Ricerca Scientifica snc, 00133 Roma, Italy.
The ability of magnetic fields (MFs) to promote/increase Ca(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(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(2+) mobilization from endoplasmic reticulum, but significantly increase the resulting Ca(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(2+) entry (NCCE), a type of influx with an inherent signaling function, rather than a capacitative Ca(2+) entry (CCE). All treatments abrogating the extra Ca(2+) influx also abrogate the anti-apoptotic effect of MFs, demonstrating that MF-induced NCCE elicits an anti-apoptotic survival pathway.