Document Detail


Electromagnetic field therapy delays cellular senescence and death by enhancement of the heat shock response.
MedLine Citation:
PMID:  18325704     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Felipe P Perez; Ximing Zhou; Jorge Morisaki; Donald Jurivich
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.     Date:  2008-01-29
Journal Detail:
Title:  Experimental gerontology     Volume:  43     ISSN:  0531-5565     ISO Abbreviation:  Exp. Gerontol.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-17     Completed Date:  2008-10-14     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0047061     Medline TA:  Exp Gerontol     Country:  England    
Other Details:
Languages:  eng     Pagination:  307-16     Citation Subset:  IM    
Affiliation:
Department of Medicine and Section of Geriatric Medicine, University of Illinois Mail Code 717, College of Medicine, Chicago, IL 60612, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Cell Aging / radiation effects*
Cell Death / radiation effects*
DNA-Binding Proteins / metabolism
Electromagnetic Fields*
Fibroblasts / metabolism,  radiation effects
HSP70 Heat-Shock Proteins / metabolism
Heat-Shock Response / radiation effects*
Humans
Mice
Mice, Knockout
Middle Aged
Radiation Dosage
T-Lymphocytes / metabolism,  radiation effects
Transcription Factors / metabolism
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/HSP70 Heat-Shock Proteins; 0/Transcription Factors; 0/heat shock transcription factor

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