Fig. 5: CLU-induced OPC injuries were attenuated by VLDLR knockdown in vivo.

A, B NG2-shRNA-mediated VLDLR knockdown efficiency was determined by Western blot (n = 3 technical replicates/group, p = 0.0005). C Schematic of viral constructs and representation of the experimental setup. D–F The reductions of NG2+ OPCs and Edu+ OPCs in the CLU-administered group were reversed by VLDLR’s specific knockdown of OPCs (n = 3 mice/group, p = 0.0035; p = 0.0083). G, H The increase of CC3+ OPCs in the CLU-administered group was reversed by VLDLR’s specific knockdown of OPCs (n = 3 mice/group, p = 0.0070). For immunofluorescence pictures: Scale bar: 50 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. VLDLR very low-density lipoprotein receptor.