Physiol. Genomics AJP: Renal Physiology
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Physiol. Genomics 7: 201-213, 2001. First published November 15, 2001; doi:10.1152/physiolgenomics.00074.2001
1094-8341/01 $5.00
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Received 4 September 2001; accepted in final form 7 November 2001.
Physiological Genomics 7:201-213 (2001)
1094-8341/01 $5.00 © 2001 American Physiological Society

Gene expression profiling of acute spinal cord injury reveals spreading inflammatory signals and neuron loss

JASON B. CARMEL1, ANTHONY GALANTE3, PATRICIA SOTEROPOULOS3, PETER TOLIAS3, MICHAEL RECCE4, WISE YOUNG1 and RONALD P. HART1,2

1 W. M. Keck Center for Collaborative Neuroscience, Rutgers University, Piscataway 08854
2 Department of Biological Sciences, Rutgers University, Newark, NJ 07102
3 Center for Applied Genomics, Public Health Research Institute and University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103
4 Center for Computational Biology and Bioengineering, New Jersey Institute of Technology, Newark, New Jersey 07103

We have completed the first large-scale gene expression study of acute spinal cord injury (SCI) in rat. Oligonucleotide microarrays containing 1,200 gene-specific probes were used to quantify mRNA levels, relative to uninjured controls, in spinal cords injured using a standard contusion model. Our results revealed a marked loss of neuron-specific mRNAs at the injury site. The surviving cells showed a characteristic inflammatory response that started at the injury site and spread to the distal cord. Changes in several mRNA levels were associated with putative regenerative responses in the spinal cord. Notably, phosphodiesterase 4, nestin, glia-derived neurite promoting factor, and GAP-43 mRNAs increased significantly. Other mRNAs clustered temporally and spatially with these regeneration-associated genes. Thus we have described global patterns of gene expression following acute SCI, and we have identified targets for future study and possible therapeutic intervention.

spinal cord injury; microarray; gene expression; regeneration-associated genes; inflammation; cell death




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