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J. Biol. Chem., Vol. 280, Issue 3, 2084-2091, January 21, 2005

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In Vivo and in Vitro Characterization of Novel Neuronal Plasticity Factors Identified following Spinal Cord Injury^*

Simone Di Giovanni¶||, Andrea De Biase¶, Alexander Yakovlev, Tom Finn, Jeanette Beers, Eric P. Hoffman, and Alan I. Faden**

From the Department of Neuroscience, Georgetown University Medical Center, Washington D. C. 20057 and the Center for Genetic Medicine, Children's National Medical Center, Washington D. C. 20010

Following spinal cord injury, there are numerous changes in gene expression that appear to contribute to either neurodegeneration or reparative processes. We utilized high density oligonucleotide microarrays to examine temporal gene profile changes after spinal cord injury in rats with the goal of identifying novel factors involved in neural plasticity. By comparing mRNA changes that were coordinately regulated over time with genes previously implicated in nerve regeneration or plasticity, we found a gene cluster whose members are involved in cell adhesion processes, synaptic plasticity, and/or cytoskeleton remodeling. This group, which included the small GTPase Rab13 and actin-binding protein Coronin 1b, showed significantly increased mRNA expression from 7–28 days after trauma. Overexpression in vitro using PC-12, neuroblastoma, and DRG neurons demonstrated that these genes enhance neurite outgrowth. Moreover, RNAi gene silencing for Coronin 1b or Rab13 in NGF-treated PC-12 cells markedly reduced neurite outgrowth. Coronin 1b and Rab13 proteins were expressed in cultured DRG neurons at the cortical cytoskeleton, and at growth cones along with the pro-plasticity/regeneration protein GAP-43. Finally, Coronin 1b and Rab13 were induced in the injured spinal cord, where they were also co-expressed with GAP-43 in neurons and axons. Modulation of these proteins may provide novel targets for facilitating restorative processes after spinal cord injury.

Received for publication, October 21, 2004 , and in revised form, November 1, 2004.

^* This work was supported by National Institutes of Health Contract NIH-NINDS-01 (NS-1-2339) (to A. I. F. and E. P. H.), and a National Institutes of Health Programs in Genomic Applications Grant U01 HL66614 HOPGENE (to E. P. H.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ These authors equally contributed to this work.

^|| To whom correspondence may be addressed: Dept. of Neuroscience, Georgetown University School of Medicine, 3900 Reservoir Rd., NW, Washington, D. C. 20057. E-mail: sd69{at}georgetown.edu. ** To whom correspondence may be addressed: Dept. of Neuroscience, Georgetown University School of Medicine, 3900 Reservoir Rd., NW, Washington, D. C. 20057. E-mail: fadena{at}georgetown.edu.

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