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. 2023 May 5;9(18):eadd2676. doi: 10.1126/sciadv.add2676

Fig. 1. TMEM106B deficiency leads to increased demyelination after CPZ treatment and impaired remyelination during recovery.

Fig. 1.

(A to D) Ten-week-old WT mice and Tmem106b−/− mice (KO) mice were fed with normal chow (ND) or CPZ-containing chow for 5 weeks (CPZ 5w). Another group of mice was fed with normal chow for 3 weeks after 5 weeks of CPZ treatment (Rec 3w). Brain sections were stained with MBP and PLP antibodies. Representative images from the corpus callosum region and frontal cortex were shown. Scale bars, 100 μm. MBP and PLP intensities were quantified in (B) and (D), respectively. Data represent the means ± SEM. Statistical significance was analyzed by two-way ANOVA (n = 3 to 4 mice per group). ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. (E to G) WT and KO mice were fed with normal chow for 3 weeks after 5 weeks of CPZ treatment (Rec 3w). Brain sections were stained with antibodies against APC and OLIG2. Representative images from the corpus callosum region were shown. Scale bars, 100 μm. The total number of mature oligodendrocytes (OLs) (APC+/OLIG2+) at different time points was quantified in (F). Data represent the means ± SEM. Statistical significance was analyzed by two-way ANOVA (n = 3 to 4 mice per group). *P < 0.05; **P < 0.01; ****P < 0.0001. The ratio of mature OLs (APC+/OLIG2+) and total OLs (OLIG2+) was quantified in (G). Data were analyzed by unpaired two-tailed Student’s t test (n = 3 mice per group). **P < 0.01.