Additional file 9: Figure S7. of Systemic inflammation disrupts oligodendrocyte gap junctions and induces ER stress in a model of CNS manifestations of X-linked Charcot-Marie-Tooth disease

LPS disrupts oligodendrocyte GJs formed by Cx47 in spinal cord gray matter. a-f: Fixed longitudinal spinal cord gray matter sections immunostained with oligodendrocyte marker CC1 (green) and Cx47 (red) and counterstained with DAPI (blue). In KO T55I tissues all oligodendrocytes transgenically express EGFP and were not stained with CC1. Cx47 immunoreactivity and GJ plaque formation at oligodendrocyte cell bodies and proximal processes is reduced in LPS-treated mice (b, d, f) of all genotypes compared to their saline controls (a, c, e). Scale bar: 20 μm. Counts of Cx47 GJ plaques per individual oligodendrocyte shows a significant reduction in LPS compared to saline treated mice (h, j, l), whereas the number of CC1/EGFP-positive oligodendrocytes per genotype as indicated shows no significant reduction in LPS compared to saline treated mice (Student’s t-test, *:p < 0.05, **:p < 0.01, ***:p < 0.001). (TIF 8996 kb)