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Figure 6 | BMC Genomics

Figure 6

From: The human G93A-SOD1 mutation in a pre-symptomatic rat model of amyotrophic lateral sclerosis increases the vulnerability to a mild spinal cord compression

Figure 6

Gene candidates showing a significant differential regulation comparing the G93A-SOD1 to the WT spinal cord after mild compression SCI. 31 gene candidates have been found to have a significant level of differential expression comparing G93A-SOD1 and WT naïve spinal cord tissues at 10 weeks of age (*) and the same tissues at different time points after mild compression SCI (Bead-array analysis). Each gene's differential regulation is further characterised by comparing the injured spinal cord tissue with genetically-matched naive spinal cord tissue and reported as fold changes of the ratio injured/naïve tissues. The genes are sub-divided according to whether their expression change occurs in WT spinal cord, in G93A-SOD1 spinal cord or in both (genes reported in bold) and to whether their expression increases (↑) or decreases (↓) compared to naïve genetically-matched spinal cord tissues. The majority of genes showing differential expression after SCI are identified in the 24 hours and in the 7 days time points. Mapb1, Hcn2 and Mast1 (reported in bold) are differentially regulated in both WT and G93A-SOD1 spinal cords and the differential regulation seems to go in the opposite way for each gene candidate in the two tissues in study when genetically age-matched naive tissue is used as reference. The GO categories which include the differentially regulated genes are also reported (in bold those already identified by GoMiner ontological analysis, Figure 2). *: Nfh expression appears to decrease significantly in the WT spinal cord at 24 hours and 7 days from compression SCI, compared to age-matched and genetically-matched naïve spinal cord.

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