Effects of 50 Hz electromagnetic fields on voltage-gated Ca2+ channels and their role in modulation of neuroendocrine cell proliferation and death.

Author: Grassi C1, D'Ascenzo M, Torsello A, Martinotti G, Wolf F, Cittadini A, Azzena GB.
Affiliation: 1Institute of Human Physiology, Medical School, Catholic University S. Cuore, Largo F. Vito 1, 00168 Rome, Italy. grassi@rm.unicatt.it
Conference/Journal: Cell Calcium.
Date published: 2004 Apr
Other: Volume ID: 35 , Issue ID: 4 , Pages: 307-15 , Word Count: 189


Abstract
Possible correlation between the effects of electromagnetic fields (EFs) on voltage-gated Ca(2+) channels, cell proliferation and apoptosis was investigated in neural and neuroendocrine cells. Exposure to 50 Hz EFs significantly enhanced proliferation in human neuroblastoma IMR32 (+40%) and rat pituitary GH3 cells (+38%). In IMR32 cells EF stimulation also inhibited puromycin- and H(2)O(2)-induced apoptosis (-22 and -33%, respectively). EF effects on proliferation and apoptosis were counteracted by Ca(2+) channel blockade. In whole-cell patch-clamp experiments 24-72 h exposure to EFs increased macroscopic Ba(2+)-current density in both GH3 (+67%) and IMR32 cells (+40%). Single-channel recordings showed that gating of L and N channels was instead unaffected, thus suggesting that the observed enhancement of current density was due to increased number of voltage-gated Ca(2+) channels. Western blot analysis of plasma membrane-enriched microsomal fractions of GH3 and IMR32 cells confirmed enhanced expression of Ca(2+) channel subunit alpha(1) following exposure to EFs. These data provide the first direct evidence that EFs enhance the expression of voltage-gated Ca(2+) channels on plasma membrane of the exposed cells. The consequent increase in Ca(2+) influx is likely responsible for the EF-induced modulation of neuronal cell proliferation and apoptosis.
PMID: 15036948