TRANSCRIPTOME 2002: From Functional Genomics to Systems Biology
March 10-13, 2002
Seattle, Washington, USA


Pathogenic Pathways in Spinal Cord Injury Identified by Gene Expression Profiling

Simone Di Giovanni1,2; Susan Knoblach2, Cinzia Brandoli1, Alan Faden2, Eric Hoffman1, 1Childrens National Medical Center, Center for Genetic Medicine, Washington, DC, 2Georgetown University Medical Center Laboratory for the Study of Central Nervous System Injury Department of Neuroscience Washington, DC

Spinal cord injury is a major cause of disability, and it is known that much of the functional deficit results from delayed cellular consequences of injury repair mechanisms.  To define the temporal series of gene expression changes following a spinal cord injury, rats were subjected to a controlled mild injury by weight drop.  Rats were sacrificed at four time points (30 min, 4h, 24h and 7 days), with 4 to 6 individual rat spinal cords expression profiled at each time point (total 26 U34A profiles).   Genes showing forty or more “present” calls in 26 profiles by Affymetrix analyses were retained for further analysis (data scrubbing), and p values and fold changes correlated, with temporal and functional clustering.  Specific RNAs were verified by QMF-RT-PCR using infrared primers, and by immunocytochemistry.  We found rapid induction of immediate early genes (30 min), followed by induction of DNA damage-inducible genes and cell cycle related genes.  The profile of the cell cycle genes suggested favoring the G1 to S transition (4 and 24h). Inflammatory and oxidative stress genes were upregulated in all profiles.  We conclude that DNA damage and cell cycle related genes seem to be important in both cellular apoptosis (glia and neurons) and in proliferation (glia cells) as shown by their localization in both degenerating and proliferating glia and damaged neurons.

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