Autophagy is modulated in human neuroblastoma cells through direct exposition to low frequency electromagnetic fields.

Abstract

In neurogenerative diseases, comprising Alzheimer's (AD), functional alteration in autophagy is considered one of the pathological hallmarks and a promising therapeutic target. Epidemiological investigations on the possible causes undergoing these diseases have suggested that electromagnetic fields (EMF) exposition can contribute to their etiology. On the other hand, EMF have therapeutic implications in reactivating neuronal functionality. To partly clarify this dualism, the effect of low-frequency EMF (LF-EMF) on the modulation of autophagy was investigated in human neuroblastoma SH-SY5Y cells, which were also subsequently exposed to Aβ peptides, key players in AD. The results primarily point that LF-EMF induce a significant reduction of microRNA 30a (miR-30a) expression with a concomitant increase of Beclin1 transcript (BECN1) and its corresponding protein. Furthermore, LF-EMF counteract the induced miR-30a up-regulation in the same cells transfected with miR-30a mimic precursor molecules and, on the other side, rescue Beclin1 expression after BECN1 siRNA treatment. The expression of autophagy-related markers (ATG7 and LC3B-II) as well as the dynamics of autophagosome formation were also visualized after LF-EMF exposition. Finally, different protocols of repeated LF-EMF treatments were assayed to contrast the effects of Aβ peptides in vitro administration. Overall, this research demonstrates, for the first time, that specific LF-EMF treatments can modulate in vitro the expression of a microRNA sequence, which in turn affects autophagy via Beclin1 expression. Taking into account the pivotal role of autophagy in the clearance of protein aggregates within the cells, our results indicate a potential cytoprotective effect exerted by LF-EMF in neurodegenerative diseases such as AD. J. Cell. Physiol. 229: 1776-1786, 2014. © 2014 Wiley Periodicals, Inc.

• Authors: Nicoletta Marchesi, Cecilia Osera, Lorenzo Fassina, Marialaura Amadio, Francesca Angeletti, Martina Morini, Giovanni Magenes, Letizia Venturini, Marco Biggiogera, Giovanni Ricevuti, Stefano Govoni, Salvatore Caorsi, Alessia Pascale, Sergio Comincini
• Journal: Journal of cellular physiology (J Cell Physiol) Vol. 229 Issue 11 Pg. 1776-86 (Nov 2014) ISSN: 1097-4652 [Electronic] United States
• PMID: 24676932 (Publication Type: Journal Article)
• Copyright: © 2014 Wiley Periodicals, Inc.

Chemical References

• Amyloid beta-Peptides
• Apoptosis Regulatory Proteins
• BECN1 protein, human
• Beclin-1
• Biomarkers
• MAP1LC3B protein, human
• MIRN30b microRNA, human
• Membrane Proteins
• MicroRNAs
• Microtubule-Associated Proteins
• Green Fluorescent Proteins

Topics

• Amyloid beta-Peptides (toxicity)
• Apoptosis Regulatory Proteins (genetics, metabolism)
• Autophagy (drug effects, genetics)
• Beclin-1
• Biomarkers (metabolism)
• Cell Line, Tumor
• Cell Survival (drug effects, genetics)
• Electromagnetic Fields
• Gene Expression Regulation, Neoplastic (drug effects)
• Green Fluorescent Proteins (metabolism)
• Humans
• Membrane Proteins (genetics, metabolism)
• MicroRNAs (genetics, metabolism)
• Microtubule-Associated Proteins (metabolism)
• Neuroblastoma (genetics, pathology, ultrastructure)