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Brain Advance Access originally published online on August 29, 2007
Brain 2007 130(11):2962-2976; doi:10.1093/brain/awm200
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© The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Expression of FGF-2 in neural progenitor cells enhances their potential for cellular brain repair in the rodent cortex

Alexandre G. Dayer1,2,*, Benoit Jenny1,3,*, Marc-Olivier Sauvain4, Gael Potter1, Patrick Salmon1, Eloisa Zgraggen1, Michiko Kanemitsu1, Eduardo Gascon1, Stephane Sizonenko1, Didier Trono4 and Jozsef Z. Kiss1

1Department of Neurosciences, University Medical Center, University of Geneva Medical School, Departments of 2Adult Psychiatry and 3Neurosurgery, University Hospital of Geneva, CH-1211 Geneva 4 and 4School of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland

Correspondence to: Jozsef Zoltan Kiss, Department of Neurosciences, University Medical Center (CMU), Rue Michel-Servet 1, 1211 Genève 4, Switzerland E-mail: Jozsef.Kiss{at}medecine.unige.ch

Strategies to enhance the capacity of grafted stem/progenitors cells to generate multipotential, proliferative and migrating pools of cells in the postnatal brain could be crucial for structural repair after brain damage. We investigated whether the over-expression of basic fibroblast growth factor 2 (FGF-2) in neural progenitor cells (NPCs) could provide a robust source of migrating NPCs for tissue repair in the rat cerebral cortex. Using live imaging we provide direct evidence that FGF-2 over-expression significantly enhances the migratory capacity of grafted NPCs in complex 3D structures, such as cortical slices. Furthermore, we show that the migratory as well as proliferative properties of FGF-2 over-expressing NPCs are maintained after in vivo transplantation. Importantly, after transplantation into a neonatal ischaemic cortex, FGF-2 over-expressing NPCs efficiently invade the injured cortex and generate an increased pool of immature neurons available for brain repair. Differentiation of progenitor cells into immature neurons was correlated with a gradual down-regulation of the FGF-2 transgene. These results reveal an important role for FGF-2 in regulating NPCs functions when interacting with the host tissue and offer a potential strategy to generate a robust source of migrating and immature progenitors for repairing a neonatal ischaemic cortex.

Key Words: Brain repair; neonatal ischemia; neural progenitors; transplantation; migration; FGF-2

Abbreviations: DCX, doublecortin; DIV, days in vitro; GABA, ({gamma}-aminobutyric acid; GAD-67, glutamic acid decarboxylase 67; NPCs, neural progenitor cells; SVZ, subventricular zone; TU, transducing units

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Received May 17, 2007. Revised July 20, 2007. Accepted August 2, 2007.

*These authors contributed equally to this work.


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