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Research Article

Transplantation of human glial-restricted neural precursors into injured spinal cord promotes functional and sensory recovery without causing allodynia

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Pages 61-68 | Received 03 Nov 2009, Accepted 19 Jul 2010, Published online: 24 Aug 2010
 

Abstract

Background aims. Traumatic injuries of the central nervous system cause damage and degeneration of specific cell populations with subsequent functional loss. Cell transplantation is a strategy to treat such injuries by replacing lost or damaged cell populations. Many kinds of cells are considered candidates for intraspinal transplantation. Human neural precursor cells (hNPC) derived from post-mortem fetal tissue are easy to isolate and expand, and are capable of producing large numbers of neuronal and glial cells. After transplantation into the nervous system, hNPC produce mature neural phenotypes and permit functional improvement in some models of neurodegenerative disease. In this study, we aimed to elucidate the therapeutic effect of different neuronal and glial progenitor populations of hNPC on locomotor and sensory functions of spinal cord-injured (SCI) rats. Methods. Different populations of progenitor cells were obtained from hNPC by cell sorting and neural induction, resulting in cell cultures that were NCAM+ A2B5+, NCAM+ A2B5 or A2B5+ NG2+. These different cell populations were then tested for efficacy in repair of the injured spinal cord by transplantation into rats with SCI. Results. The A2B5+ NG2+ population of hNPC significantly improved locomotor and sensory (hindlimb) functional recovery of SCI rats. Importantly, no abnormal pain responses were observed in the forelimbs following transplantation. Conclusions. This treatment approach can improve functional recovery after SCI without causing allodynia. Further studies will be conducted to investigate the ability of A2B5+ NG2+ cells to survive, differentiate and integrate in the injured spinal cord.

Acknowledgements

This work was supported by Veteran's Affairs Merit Review grant.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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