Neurochemical Research

, Volume 32, Issue 2, pp 353–362

Human Mesenchymal Stem Cells Signals Regulate Neural Stem Cell Fate

Authors

  • Lianhua Bai
    • Centers for Stem Cells and Regenerative Medicine, Translational Neuroscience, Department of Neurosciences, Case School of MedicineCase Western Reserve University
  • Arnold Caplan
    • Skeletal Research CenterCase Western Reserve University
  • Donald Lennon
    • Skeletal Research CenterCase Western Reserve University
    • Centers for Stem Cells and Regenerative Medicine, Translational Neuroscience, Department of Neurosciences, Case School of MedicineCase Western Reserve University
Original Paper

DOI: 10.1007/s11064-006-9212-x

Cite this article as:
Bai, L., Caplan, A., Lennon, D. et al. Neurochem Res (2007) 32: 353. doi:10.1007/s11064-006-9212-x

Abstract

Neural stem cells (NSCs) differentiate into neurons, astrocytes and oligodendrocytes depending on their location within the central nervous system (CNS). The cellular and molecular cues mediating end-stage cell fate choices are not completely understood. The retention of multipotent NSCs in the adult CNS raises the possibility that selective recruitment of their progeny to specific lineages may facilitate repair in a spectrum of neuropathological conditions. Previous studies suggest that adult human bone marrow derived mesenchymal stem cells (hMSCs) improve functional outcome after a wide range of CNS insults, probably through their trophic influence. In the context of such trophic activity, here we demonstrate that hMSCs in culture provide humoral signals that selectively promote the genesis of neurons and oligodendrocytes from NSCs. Cell–cell contacts were less effective and the proportion of hMSCs that could be induced to express neural characteristics was very small. We propose that the selective promotion of neuronal and oligodendroglial fates in neural stem cell progeny is responsible for the ability of MSCs to enhance recovery after a wide range of CNS injuries.

Keywords

Neural stem cells MSCs Migration Differentiation Neurons Oligodendrocytes

Copyright information

© Springer Science+Business Media, LLC 2006