Fig. 8: Improved myelin renewal with astrocyte-specific CLU conditional knockout in LPC and EAE models.

A Schematic representation of the ALDH1L1-CreERT:: CLU^fl/fl mice construction. B–D Increased numbers of Olig2⁺ OPCs and CC1⁺ OLs in the corpus callosum of CLU cKO^AST mice in the LPC model (n = 3 mice/group, p = 0.0013; p = 0.0004). E–H TEM analyses revealed thicker myelin sheaths in CLU cKO^AST mice compared to CLU^fl/fl mice. The percentage of unmyelinated axons decreased in CLU cKO^AST mice compared to the CLU^fl/fl group (n = 3 mice/group, p = 0.0052), while the axon diameter remained consistent (n = 3 mice/group, p = 0.8429). I Astrocyte-specific CLU conditional knockout decreased the clinical severity of EAE animals (n = 6 mice/group). J–L Astrocyte-specific CLU conditional knockout increased the number of NG2⁺ OPCs at the peak of the disease onset, while the number of Ki67+ OPCs was unchanged (n = 5 mice/group, p = 0.0005; p = 0.9679). M, N Astrocyte-specific CLU conditional knockout increased the number of CC3⁺ OPCs at the peak of the disease onset (n = 5 mice/group, p < 0.0001). For immunofluorescence pictures: Scale bar: 50 μm. For TEM Scale bar: 1 μm. Statistical analysis was performed using unpaired two-tailed Student’s t-tests, mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.001. ns. = p not significant. LPC lysolecithin.