title: 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.
authors.affiliation: Department of Medicine and Section of Geriatric Medicine, University of Illinois Mail Code 717, College of Medicine, Chicago, IL 60612, USA.
authors.forename: Felipe P
authors.initials: FP
authors.lastname: Perez
authors.forename: Ximing
authors.initials: X
authors.lastname: Zhou
authors.forename: Jorge
authors.initials: J
authors.lastname: Morisaki
authors.forename: Donald
authors.initials: D
authors.lastname: Jurivich
mesh_terms: D000328:Adult; D000818:Animals; D016923:Cell Death / Q000528:radiation effects*; D016922:Cellular Senescence / Q000528:radiation effects*; D004268:DNA-Binding Proteins / Q000378:metabolism; D004574:Electromagnetic Fields; D005347:Fibroblasts / Q000378:metabolism / Q000528:radiation effects; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D000076249:Heat Shock Transcription Factors; D018869:Heat-Shock Response / Q000528:radiation effects*; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008875:Middle Aged; D011829:Radiation Dosage; D013601:T-Lymphocytes / Q000378:metabolism / Q000528:radiation effects; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; C000619706:HSF1 protein, human; D018840:HSP70 Heat-Shock Proteins; D000076249:Heat Shock Transcription Factors; D014157:Transcription Factors