Cytoprotective response induced by electromagnetic stimulation on SH-SY5Y human neuroblastoma cell line

Tissue Eng Part A. 2011 Oct;17(19-20):2573-82. doi: 10.1089/ten.TEA.2011.0071. Epub 2011 Jul 5.

Abstract

It is well known that physiological functions and pathological conditions of cells and tissues can be influenced not only by chemical molecules, but also by physical stimuli such as electromagnetic waves. In particular, epidemiological studies suggest possible associations between exposure to electromagnetic fields and an increased risk of tumors and neurodegenerative disorders, such as Alzheimer's disease. However, depending on the dose and on the length of treatment, the electromagnetic stimuli can be harmful or induce a cytoprotective cellular response, suggesting a possible application in medical therapy. In this study, under a tissue engineering viewpoint, we investigated the effects of an electromagnetic wave (magnetic field intensity, 2 mT; frequency, 75 Hz) on a neuronal cellular model characterized by the overexpression of the amyloid precursor protein (APP). After a prolonged electromagnetic treatment, lower mitochondrial activity and proliferation rate, resulting in a higher cellular quiescence, were observed. Focusing on the stress and oxidative pathways, we detected an overall increase of two fundamental proteins, the chaperone heat shock protein HSP70 and the free radical scavenger superoxide dismutase-1 enzyme (SOD-1). Interestingly, we found that the electromagnetic stimulation promotes the nonamyloidogenic processing of APP through an increased expression of the α-secretase ADAM10 and an enhanced release of the soluble neurotrophic factor sAPPα (a product of the ADAM10-mediated cleavage of APP). In conclusion, these findings suggest that the electromagnetic stimulus, if properly administered in terms of dose and timing, is able to induce a cytoprotective response in the cell. Moreover, these results suggest a possible use of this particular physical stimulation to improve the functional capability of the cells to face noxae.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADAM Proteins / metabolism
  • ADAM10 Protein
  • Amyloid Precursor Protein Secretases / metabolism
  • Amyloid beta-Protein Precursor / pharmacology
  • Bioreactors
  • Blotting, Western
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cytoprotection / drug effects*
  • Cytoprotection / radiation effects*
  • Electromagnetic Radiation*
  • HSP70 Heat-Shock Proteins / metabolism
  • Humans
  • Membrane Proteins / metabolism
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Neuroblastoma / enzymology
  • Neuroblastoma / pathology*
  • Protective Agents / pharmacology*
  • Superoxide Dismutase / metabolism

Substances

  • Amyloid beta-Protein Precursor
  • HSP70 Heat-Shock Proteins
  • Membrane Proteins
  • Protective Agents
  • Superoxide Dismutase
  • Amyloid Precursor Protein Secretases
  • ADAM Proteins
  • ADAM10 Protein
  • ADAM10 protein, human