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Stem Cells International
Volume 2012 (2012), Article ID 387513, 16 pages
http://dx.doi.org/10.1155/2012/387513
Review Article

Endogenous Proliferation after Spinal Cord Injury in Animal Models

1Department of Pathology and Laboratory Medicine, UC Davis, School of Medicine, 4400 V Street, Sacramento, CA 95817, USA
2Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, 2425 Stockton Boulevard, Sacramento, CA 95817, USA
3Biochemistry, Molecular, Cellular and Developmental Biology Graduate Group, UC Davis, One Shields Avenue, Davis, CA 95616, USA

Received 3 August 2012; Revised 6 October 2012; Accepted 29 October 2012

Academic Editor: Branden R. Nelson

Copyright © 2012 Ashley McDonough and Verónica Martínez-Cerdeño. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Spinal cord injury (SCI) results in motor and sensory deficits, the severity of which depends on the level and extent of the injury. Animal models for SCI research include transection, contusion, and compression mouse models. In this paper we will discuss the endogenous stem cell response to SCI in animal models. All SCI animal models experience a similar peak of cell proliferation three days after injury; however, each specific type of injury promotes a specific and distinct stem cell response. For example, the transection model results in a strong and localized initial increase of proliferation, while in contusion and compression models, the initial level of proliferation is lower but encompasses the entire rostrocaudal extent of the spinal cord. All injury types result in an increased ependymal proliferation, but only in contusion and compression models is there a significant level of proliferation in the lateral regions of the spinal cord. Finally, the fate of newly generated cells varies from a mainly oligodendrocyte fate in contusion and compression to a mostly astrocyte fate in the transection model. Here we will discuss the potential of endogenous stem/progenitor cell manipulation as a therapeutic tool to treat SCI.