The expression of PHOX2A, PHOX2B and of their target gene dopamine-beta-hydroxylase (DbetaH) is not modified by exposure to extremely-low-frequency electromagnetic field (ELF-EMF) in a human neuronal model

Toxicol In Vitro. 2008 Sep;22(6):1489-95. doi: 10.1016/j.tiv.2008.05.003. Epub 2008 May 17.

Abstract

The homeodomain transcription factors PHOX2A and PHOX2B are vital for development of the autonomic nervous system. Their spatial and temporal expression at the neural crest is instrumental in determining neuronal precursor fate, and by regulating DbetaH expression, the enzyme catalysing noradrenaline synthesis from dopamine, they also play a role in determination of noradrenergic phenotype. Disturbing this finely regulated process leads to disruption of autonomic development and autonomic dysfunction syndromes such as DbetaH deficiency. As it had previously been shown that the catecholamine system is responsive to ELF-EMF, and as this has also been linked to various pathologies and to certain types of cancer, we wondered whether exposure to this type of radiation could affect the expression of PHOX2A, PHOX2B and DbetaH, also during differentiation triggered by retinoic acid. To investigate this possibility we exposed the human SH-SY5Y neuroblastoma cell line to 50 Hz power-line magnetic field at various flux densities and for various exposure times. We measured gene expression in exposed cells compared to control cells and also investigated any changes at protein level. Using our exposure protocol, we found no changes at either transcript or protein level of these important components of the autonomic nervous system and catecholaminergic system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Dopamine beta-Hydroxylase / radiation effects
  • Electromagnetic Fields / adverse effects*
  • Gene Expression / radiation effects*
  • Homeodomain Proteins / radiation effects*
  • Humans
  • Neuroblastoma / metabolism
  • Time Factors
  • Transcription Factors / radiation effects*
  • Transcription, Genetic / radiation effects
  • Tretinoin / pharmacology

Substances

  • Homeodomain Proteins
  • NBPhox protein
  • PHOX2A protein, human
  • Transcription Factors
  • Tretinoin
  • Dopamine beta-Hydroxylase