Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8325307 | The International Journal of Biochemistry & Cell Biology | 2011 | 8 Pages |
Abstract
The ability of magnetic fields (MFs) to promote/increase Ca2+ influx into cells is widely recognized, but the underlying mechanisms remain obscure. Here we analyze how static MFs of 6Â mT modulates thapsigargin-induced Ca2+ movements in non-excitable U937 monocytes, and how this relates to the anti-apoptotic effect of MFs. Magnetic fields do not affect thapsigargin-induced Ca2+ mobilization from endoplasmic reticulum, but significantly increase the resulting Ca2+ 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 Ca2+ entry (NCCE), a type of influx with an inherent signaling function, rather than a capacitative Ca2+ entry (CCE). All treatments abrogating the extra Ca2+ influx also abrogate the anti-apoptotic effect of MFs, demonstrating that MF-induced NCCE elicits an anti-apoptotic survival pathway.
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Authors
Claudia Cerella, Sonia Cordisco, Maria Cristina Albertini, Augusto Accorsi, Marc Diederich, Lina Ghibelli,