Fig. 8: PI-88 treatment accelerated OL differentiation via inhibition of Sulf1/2 following demyelination.

Wild-type (WT) and Sulf1/2 cKO mice underwent focal spinal cord demyelination with or without PI-88 injection and were sacrificed at 7 days post lesion. a–d Olig2 (green)/CC1 (red) immunofluorescence. e–l Confocal RNAscope in situ hybridization for OPC-expressed Pdgfra (red) and either WNT target gene Apcdd1 (green, e–h) or BMP target gene Id4 (green, i–l). Arrows indicate double-labeled OPCs. m–o Quantification of oligodendrocyte lineage density (Olig2⁺, m) (n = 4 mice for WT, n = 5 mice for Sulf1/2 cKO groups), postmitotic CC1⁺Olig2⁺ cells (n) (n = 4 mice per group), and percentage of CC1⁺ cells within the Olig2 population (o) (n = 4 mice per group). Quantification of WNT pathway activity Appcd1% (p) (n = 5 mice for control WT and PI-88 treated WT, n = 6 for control Sulf1/2 cKO, and n = 4 for PI-88 treated Sulf1/2 cKO) and BMP pathway activity Id4% (q) (n = 4 mice for control WT and PI-88 treated Sulf1/2 cKO groups and n = 5 for PI-88 treated WT and control Sulf1/2 cKO groups) among Pdgfra⁺ OPCs. Mean ± SEM is shown. *, **, ***, and **** indicate two-way ANOVA Holm–Sidak post-test p < 0.05, <0.01, <0.001, and <0.0001, respectively. Scale: 20 µm.