Induction of heat shock gene expression in RAT1 primary fibroblast cells by ELF electric fields
Article first published online: 1 MAR 2013
Copyright © 2013 Wiley Periodicals, Inc.
Volume 34, Issue 5, pages 405–413, July 2013
How to Cite
Frisch, P., Li, G. C., McLeod, K. and Laramee, C. B. (2013), Induction of heat shock gene expression in RAT1 primary fibroblast cells by ELF electric fields. Bioelectromagnetics, 34: 405–413. doi: 10.1002/bem.21786
- Issue published online: 5 JUN 2013
- Article first published online: 1 MAR 2013
- Manuscript Accepted: 25 JAN 2013
- Manuscript Received: 27 JAN 2012
- electric field exposure;
- HSP70 expression;
- rat primary fibroblast (RAT1) cells
Recent studies have demonstrated that the Ku70 gene fragment can be placed in the anti-sense orientation under the control of a heat-inducible heat shock protein 70 (HSP70) promoter and activated through heat shock exposure. This results in attenuation of the Ku70 protein expression, inhibiting cellular repair processes, and sensitizing the transfected cells to exposures such as the ionizing radiation exposures used clinically. However, achieving the tissue temperatures necessary to thermally induce the HSP70 response presents significant limitations to the clinical application of this strategy. Previous findings suggest an alternative approach to inducing a heat shock response, specifically through the use of extremely low frequency (ELF) electrical field stimulation. To further pursue this approach, we investigated HSP70 responses in transfected rat primary fibroblast (RAT1) cells exposed to 10 Hz electric fields at intensities of 20–500 V/m. We confirmed that low frequency electric fields can induce HSP70 heat shock expression, with peak responses obtained at 8 h following a 2 h field exposure. However, the approximate threefold increase in expression is substantially lower than that obtained using thermal stimulation, raising questions of the clinical utility of the response. Bioelectromagnetics 34:405–413, 2013. © 2012 Wiley Periodicals, Inc.