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Neuroprotective Effect of Transplanted Neural Precursors Embedded on PLA/CS Scaffold in an Animal Model of Multiple Sclerosis

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Abstract

Multiple sclerosis (MS) is an immune-mediated demyelinating disease of the central nervous system (CNS). Cell transplantation may be an attractive therapeutic approach for MS which may promote remyelination and suppress the inflammatory process. Neural precursor cells are promising in transplantation strategies to treat an injury to the CNS, because of their ability to differentiate into neural cells. Here, we investigated the use of polylactic acid/chitosan (PLA/CS) scaffold as 3D system which increases neural cell differentiation. Nerve growth factor (NGF), basic fibroblast growth factor (bFGF), and conditioned media were employed to induce PC12 cells into neural-like cells (NLCs) on nanofibrous PLA/CS scaffold. Enhanced numbers of neural structures and staining of nestin, microtubule-associated protein (Map2), and class III β-tubulin (β3-tub) were observed with PC12-cell-seeded nanofibrous scaffolds when compared with control medium. The results revealed that PC12 cells attach, grow, and undergo differentiation on the nanofibrous PLA/CS scaffold. Additionally, our study illustrates that transplanted PC12-derived NLCs into the brain lateral ventricles of mice induced with experimental autoimmune encephalomyelitis (EAE), the animal model of MS, significantly reduced the clinical signs of EAE. Histological examination showed attenuation of the inflammatory process in transplanted animals, which was correlated with the reduction of both axonal damage and demyelination.

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Acknowledgments

We thank Student’s Scientific Research Center,  Tehran University of Medical Sciences for financial support and research assistant.

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The authors declare that they have no conflict of interest.

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Correspondence to Elham Hoveizi.

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Hoveizi, E., Tavakol, S. & Ebrahimi-Barough, S. Neuroprotective Effect of Transplanted Neural Precursors Embedded on PLA/CS Scaffold in an Animal Model of Multiple Sclerosis. Mol Neurobiol 51, 1334–1342 (2015). https://doi.org/10.1007/s12035-014-8812-8

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  • DOI: https://doi.org/10.1007/s12035-014-8812-8

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