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This Article Free via Open Access: OA OA Full Text Full Text (PDF) Supplemental Data OA All Versions of this Article: 2007-1022v1 26/8/2193    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints/Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Li, L. Articles by Wan, Q. Search for Related Content PubMed PubMed Citation Articles by Li, L. Articles by Wan, Q.

TRANSLATIONAL AND CLINICAL RESEARCH

Direct-Current Electrical Field Guides Neuronal Stem/Progenitor Cell Migration

^aDivision of Fundamental Neurobiology, Toronto Western Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada;
^bResearch Institute of Surgery and Daping Hospital, State Key Laboratory of Trauma, Burns and Combined Injury of China, Chongqing, People's Republic of China,
^cBeike Biotech Co., Ltd., Shenzhen, People's Republic of China;
^dDepartment of Physiology and Cell Biology, School of Medicine, University of Nevada, Reno, Nevada, USA

Key Words. Direct-current electrical fields • Neuronal stem/progenitor cells • Migration • N-Methyl-D-aspartate receptor • GTPase

Correspondence: Correspondence: Qi Wan, M.D., Ph.D., Department of Physiology and Cell Biology, School of Medicine, University of Nevada, Reno, Nevada 89557-0271, USA. Telephone: 775-784-4352; Fax: 775-784-6903; e-mail: qwan{at}medicine.nevada.edu

Received on December 5, 2007; accepted for publication on May 30, 2008.

First published online in STEM CELLS EXPRESS  June 12, 2008.

Direct-current electrical fields (EFs) promote nerve growth and axon regeneration. We report here that at physiological strengths, EFs guide the migration of neuronal stem/progenitor cells (NSPCs) toward the cathode. EF-directed NSPC migration requires activation of N-methyl-D-aspartate receptors (NMDARs), which leads to an increased physical association of Rho GTPase Rac1-associated signals to the membrane NMDARs and the intracellular actin cytoskeleton. Thus, this study identifies the EF as a directional guidance cue in controlling NSPC migration and reveals a role of the NMDAR/Rac1/actin signal transduction pathway in mediating EF-induced NSPC migration. These results suggest that as a safe physical approach in clinical application, EFs may be developed as a practical therapeutic strategy for brain repair by directing NSPC migration to the injured brain regions to replace cell loss.

Disclosure of potential conflicts of interest is found at the end of this article.