Cell biology of spinal cord injury and repair
Timothy M. O’Shea, Joshua E. Burda, and Michael V. Sofroniew
Department of Neurobiology, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Michael V. Sofroniew, Department of Neurobiology, David Geffen School of Medicine, University of California, 10833 Le Conte Avenue, Los Angeles, California 90095-1763, USA. Phone: 310.794.4944; Email: sofroniew@mednet.ucla.edu.
Find articles by O’Shea, T. in: JCI | PubMed | Google Scholar
Department of Neurobiology, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Michael V. Sofroniew, Department of Neurobiology, David Geffen School of Medicine, University of California, 10833 Le Conte Avenue, Los Angeles, California 90095-1763, USA. Phone: 310.794.4944; Email: sofroniew@mednet.ucla.edu.
Find articles by Burda, J. in: JCI | PubMed | Google Scholar
Department of Neurobiology, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Address correspondence to: Michael V. Sofroniew, Department of Neurobiology, David Geffen School of Medicine, University of California, 10833 Le Conte Avenue, Los Angeles, California 90095-1763, USA. Phone: 310.794.4944; Email: sofroniew@mednet.ucla.edu.
Find articles by Sofroniew, M. in: JCI | PubMed | Google Scholar
First published July 24, 2017 - More info
J Clin Invest. 2017;127(9):3259–3270. doi:10.1172/JCI90608.
Copyright © 2017, American Society for Clinical Investigation
Spinal cord injury (SCI) lesions present diverse challenges for repair strategies. Anatomically complete injuries require restoration of neural connectivity across lesions. Anatomically incomplete injuries may benefit from augmentation of spontaneous circuit reorganization. Here, we review SCI cell biology, which varies considerably across three different lesion-related tissue compartments: (a) non-neural lesion core, (b) astrocyte scar border, and (c) surrounding spared but reactive neural tissue. After SCI, axon growth and circuit reorganization are determined by neuron-cell-autonomous mechanisms and by interactions among neurons, glia, and immune and other cells. These interactions are shaped by both the presence and the absence of growth-modulating molecules, which vary markedly in different lesion compartments. The emerging understanding of how SCI cell biology differs across lesion compartments is fundamental to developing rationally targeted repair strategies.
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