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Figure 1 | Molecular Neurodegeneration

Figure 1

From: Autoimmune-induced preferential depletion of myelin-associated glycoprotein (MAG) is genetically regulated in relapsing EAE (B6 × SJL) F1 mice

Figure 1

Profound depletion of MAG levels occurs in relapsing H-2b/s mice. Dissimilar regulation of relative levels of MAG was observed between H-2b and H-2b/s mice throughout EAE. Levels of MAG in spinal cord of EAE mice were measured by western blot. Approximately 20 μg of total protein was loaded per lane. Total of 3–4 mice from H-2b/s and H-2b strains with acute and relapsing stages of the disease were analyzed. Only H-2b/s mice (3 mice) with chronic-sustained disease were examined. Representative blot of 3–4 similar experiments shows: acute – H-2b/s (13 dpi, grade 4.5), H-2b (16 dpi, grade 4); relapse – H-2b/s (21 dpi, grade 3.5, 1st relapse), H-2b (27 dpi, grade 2, 1st relapse); and chronic-sustained – H-2b/s (72 dpi, grade 2.5). Relative levels of MAG were calculated as ration to corresponding levels of GAPDH (see Fig. 4). Compared to levels in control and in H-2b mice, H-2b/s mice markedly reduced their relative levels of MAG during acute and chronic. Most profound depletion of MAG was found in relapsing H-2b/s mice. Corresponding levels of GAPDH are shown in Fig. 6. Membrane was stripped and re-probed with MOG, MBP, NF160 and PARPp85 antibodies (Fig. 2, 4, 6 and 7A).

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