Fig. 7: Enhanced remyelination in the corpus callosum with CLU knockdown in the LPC model. | Nature Communications

Fig. 7: Enhanced remyelination in the corpus callosum with CLU knockdown in the LPC model.

From: Astrocyte-derived clusterin disrupts glial physiology to obstruct remyelination in mouse models of demyelinating diseases

Fig. 7

A Schematic of viral constructs. B Schematic representation of the experimental arrangement. C–E Increased proliferation ability of OPCs following CLU knockdown (n = 3 mice/group, p = 0.0001; p = 0.0013). F–H Increased numbers of NG2+ OPCs and CC1+ OLs after CLU knockdown (n = 3 mice/group, p < 0.0001; p = 0.0005). I, J Enhanced OPC differentiation ability after CLU knockdown, detected by EdU differentiation assay (n = 3 mice/group, p = 0.0011). K, L TEM analysis revealed increased myelin sheath thickness after CLU knockdown (n = 4 mice/group, three independent experiments were conducted). M, N The percentage of unmyelinated axons was decreased in A-shCLU mice compared to the A-shNC group (n = 4 mice/group, p = 0.0037), while the axon diameter was unchanged (n = 4 mice/group, p = 0.6686). 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, EdU 5-ethynyl-2’-deoxyuridine, Brdu 5-bromo-2’-deoxyuridine.

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