Potential role of N-benzylcinnamide in inducing neuronal differentiation from human amniotic fluid mesenchymal stem cells

Neurosci Lett. 2016 Jan 1:610:6-12. doi: 10.1016/j.neulet.2015.10.050. Epub 2015 Oct 27.

Abstract

Neurodegenerative disorders are characterized by chronic and progressive loss of neurons in structure and function related to aging, such as Alzheimer's disease, the latter characterized by the degeneration of cholinergic neurons in basal forebrain connected to the cerebral cortex and hippocampus. Amniotic fluid mesenchymal stem cells (AF-MSCs) have been proposed as one of the candidates for stem cell therapy of nervous system disorders. This study demonstrates that incubation of AF-MSCs, obtained from 16 to 20 week pregnant women, with 10ng/ml bone morphogenetic protein (BMP)-9 for 48h in conditioned medium resulted in transdifferentiation to cholinergic neuronal-like cells. This phenomenon could also be obtained with N-benzylcinnamide (PT-3). Pre-treatment for 1h with 10nM PT-3 augmented BMP-9 transdifferentiation effect, elevated βIII-tubulin cell numbers and fluorescence intensity of immunoreactive ChAT, ameliorated BMP-9-related production of reactive oxygen species and enhanced anti-apoptosis status of the neuronal-like cells. The transdiffirentiation process was accompanied by increased p53 but decreased Notch1 and SIRT1 (p53 deacetylase) levels, and activation of p38, ERK1/2 MAPK, and PI3K/Akt pathways, in concert with inactivation of JNK, all of which were accentuated by PT-3 pre-treatment. These findings suggest that N-benzylcinnamide may provide a useful adjuvant in BMP-9-induced transdifferentiation of AFMSCs into ultimately cholinergic neurons.

Keywords: Alzheimer’s disease; Antioxidant; Cholinergic neuron; Differentiation; Mechanism; N-Benzylcinnamide.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amniotic Fluid / cytology*
  • Cell Transdifferentiation
  • Choline O-Acetyltransferase / metabolism
  • Cholinergic Neurons / cytology
  • Cholinergic Neurons / drug effects*
  • Cholinergic Neurons / metabolism
  • Cinnamates / pharmacology*
  • Drug Interactions
  • Enzyme Activation
  • Female
  • Growth Differentiation Factor 2 / pharmacology
  • Humans
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / drug effects*
  • Mesenchymal Stem Cells / metabolism
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Receptor, Notch1 / metabolism
  • Sirtuin 1 / metabolism
  • Tubulin / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Cinnamates
  • Growth Differentiation Factor 2
  • N-benzylcinnamide
  • Receptor, Notch1
  • TUBB3 protein, human
  • Tubulin
  • Tumor Suppressor Protein p53
  • Choline O-Acetyltransferase
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • SIRT1 protein, human
  • Sirtuin 1