Electromagnetic field therapy delays cellular senescence and death by enhancement of the heat shock response

Abstract

Hormesis may result when mild repetitive stress increases cellular defense against diverse injuries. This process may also extend in vitro cellular proliferative life span as well as delay and reverse some of the age-dependent changes in both replicative and non-replicative cells. This study evaluated the potential hormetic effect of non-thermal repetitive electromagnetic field shock (REMFS) and its impact on cellular aging and mortality in primary human T lymphocytes and fibroblast cell lines. Unlike previous reports employing electromagnetic radiation, this study used a long wave length, low energy, and non-thermal REMFS (50MHz/0.5W) for various therapeutic regimens. The primary outcomes examined were age-dependent morphological changes in cells over time, cellular death prevention, and stimulation of the heat shock response. REMFS achieved several biological effects that modified the aging process. REMFS extended the total number of population doublings of mouse fibroblasts and contributed to youthful morphology of cells near their replicative lifespan. REMFS also enhanced cellular defenses of human T cells as reflected in lower cell mortality when compared to non-treated T cells. To determine the mechanism of REMFS-induced effects, analysis of the cellular heat shock response revealed Hsp90 release from the heat shock transcription factor (HSF1). Furthermore, REMFS increased HSF1 phosphorylation, enhanced HSF1-DNA binding, and improved Hsp70 expression relative to non-REMFS-treated cells. These results show that non-thermal REMFS activates an anti-aging hormetic effect as well as reduces cell mortality during lethal stress. Because the REMFS configuration employed in this study can potentially be applied to whole body therapy, prospects for translating these data into clinical interventions for Alzheimer's disease and other degenerative conditions with aging are discussed.

EXPOSURE TO 2.45 GHz MICROWAVE RADIATION PROVOKES CEREBRAL CHANGES IN INDUCTION OF HSP-90 α/β HEAT SHOCK PROTEIN IN RAT.

“…Although various authors have associated changes in levels of expression of heat-shock proteins with exposure to non ionizing radiation [3,9,37], other authors of in vitro studies with embryos [38] and of in vivo studies attribute such changes to thermal stimuli. To our knowledge no in vivo studies have described changes in the levels and distribution of the heat shock protein HSP-90 in several rat brain regions analyzed after acute controlled exposure of the animals to 2.45 GHz at non thermal SAR in a GTEM cell (see Tables 2, 3).…”

“…Furthermore, there is a relationship between exposure to electromagnetic fields that may induce inactivation of this protein and activation of proteases that trigger apoptosis [9], with a demonstrated decrease in the cytoprotective mechanisms [37]. In this sense, the decrease in the levels of HSP-90, 24 h after exposure to radiation at most SARs in the hippocampus and entorhinal cortex suggest that the effects of non ionizing radiation may be related to a decrease in the levels of protection provided by this protein.…”

Late-Onset Alzheimer's Disease, Heating up and Foxed by Several Proteins: Pathomolecular Effects of the Aging Process

“…These molecular chaperones work in tandem with the ubiquitin-proteasome pathway for protein quality control to prevent the accumulation of abnormal proteins, including Aβ [99–100]. Interestingly, intracellular Aβ also prompts the rapid induction of stress-inducible HSP70 protein in neurons [101], most likely due to activation of HSF1 [102]. …”

Low-Frequency Pulsed Electromagnetic Field Is Able to Modulate miRNAs in an Experimental Cell Model of Alzheimer’s Disease

“…Moreover, it has been reported that EMFs can delay cellular senescence [33]. As previously shown on an AD mice model, a high-frequency EMF treatment induced an improvement of cognitive functions, ascribed to an enhanced clearance of the amyloid plaques [9].…”