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Figure 4 | BMC Genomics

Figure 4

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 4

Differential regulation in injured spinal cord tissue from WT and G93A-SOD1 rats of the intermediate neurofilament heavy chain and of genes involved in retinol metabolism according to Bead-array analysis. A. Profile of post-injury differential expression of the neurofilament heavy chain (Nfh) in the WT and in the G93A-SOD1 spinal cords (intermediate neurofilaments gene category, GO:0045104), according to the Bead-array gene expression analysis. Note the higher level of expression of the neurofilament in G93A-SOD1 spinal cord at all the post-injury time points and its significant level of down-regulation in WT spinal cord at 7 days from injury compared to naive tissue. B. The graph reports the 7 day post-injury up-regulation in WT and G93A-SOD1 injured spinal cord of genes included in the retinol metabolism gene category (GO:0042572), including retinol binding protein 1 (RBP1) and cellular retinoic acid binding protein 2 (CRABP2). The up-regulation is expressed as the ratio of intensities between injured and naive tissues. Two additional genes within the GO:0042572 gene category, the alcohol dehydrogenase 1 (ADH1) and aldehyde dehydrogenase 1, member A2 (ALDH1a2) are up-regulated only in the G93A-SOD1 spinal cord at 7 days from injury.

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