Pulsed electromagnetic fields promote survival and neuronal differentiation of human BM-MSCs

Life Sci. 2016 Apr 15;151:130-138. doi: 10.1016/j.lfs.2016.02.066. Epub 2016 Feb 17.

Abstract

Pulsed electromagnetic fields (PEMF) are known to affect biological properties such as differentiation, regulation of transcription factor and cell proliferation. However, the cell-protective effect of PEMF exposure is largely unknown. The aim of this study is to understand the mechanisms underlying PEMF-mediated suppression of apoptosis and promotion of survival, including PEMF-induced neuronal differentiation. Treatment of induced human BM-MSCs with PEMF increased the expression of neural markers such as NF-L, NeuroD1 and Tau. Moreover, treatment of induced human BM-MSCs with PEMF greatly decreased cell death in a dose- and time-dependent manner. There is evidence that Akt and Ras are involved in neuronal survival and protection. Activation of Akt and Ras results in the regulation of survival proteins such as Bad and Bcl-xL. Thus, the Akt/Ras signaling pathway may be a desirable target for enhancing cell survival and treatment of neurological disease. Our analyses indicated that PEMF exposure dramatically increased the activity of Akt, Rsk, Creb, Erk, Bcl-xL and Bad via phosphorylation. PEMF-dependent cell protection was reversed by pretreatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). Our data suggest that the PI3K/Akt/Bad signaling pathway may be a possible mechanism for the cell-protective effects of PEMF.

Keywords: Apoptosis; Human BM-MSCs; Neuronal differentiation; PEMF; Survival.

MeSH terms

  • Apoptosis / radiation effects
  • Bone Marrow Cells / radiation effects*
  • Cell Differentiation / radiation effects*
  • Cell Survival / radiation effects
  • Cyclic AMP Response Element-Binding Protein / biosynthesis
  • Cyclic AMP Response Element-Binding Protein / radiation effects
  • Dose-Response Relationship, Radiation
  • Electromagnetic Fields*
  • Mesenchymal Stem Cells / radiation effects*
  • Nerve Tissue Proteins / metabolism
  • Neural Stem Cells / radiation effects*
  • Oncogene Protein v-akt / radiation effects
  • Phosphatidylinositol 3-Kinases / radiation effects
  • Receptor, trkA / radiation effects
  • Signal Transduction / radiation effects
  • bcl-Associated Death Protein / radiation effects

Substances

  • BAD protein, human
  • Cyclic AMP Response Element-Binding Protein
  • Nerve Tissue Proteins
  • TRKA protein, human
  • bcl-Associated Death Protein
  • Phosphatidylinositol 3-Kinases
  • Receptor, trkA
  • Oncogene Protein v-akt