Figure 2

Oligodendrogenesis is increased in IκBα-dn mice lacking functional NF-κB signaling in astrocytes. (A) Mice were subjected to moderate spinal cord contusion at T9 and received bromodeoxyuridine (BrdU) injections once a day for 1 week starting 5 weeks post-injury. Spinal cord tissue (in total 2 mm centered on injury) was analyzed 7 weeks post-spinal cord injury (SCI). (B, C) The total estimated number of BrdU⁺NG2⁺ cells using Stereo Investigator software in a 2-mm segment of spinal cord centered on the site of injury was similar between wild-type (WT) and IκBα-dn mice (B) with a similar distribution over the injured spinal cord (C). (D, E) In contrast, the total estimated number of BrdU⁺CC1⁺ cells was significantly increased in IκBα-dn mice (D, *P < 0.05, Student’s t-test) with a higher number of newly formed oligodendrocytes around the epicenter compared to those in WT mice (E, two-way analysis of variance; *P<0.05 Bonferroni post-test). (F) Representative pictures of BrdU⁺NG2⁺ and Brdu⁺CC1⁺ cells showing co-labeling with the oligodendroglial lineage marker Olig2. (G, left) At this time point, the total number of mature oligodendrocyte (CC1⁺ cells) in the injured spinal cord of IκBα-dn mice was also significantly (*P < 0.05, Student’s t-test) higher than in WT mice. (G, right) Western blot quantification on mice with 6 weeks survival also showed a significant increase in the myelin protein PLP in IκBα-dn mice compared to WT mice (*P < 0.05, Student’s t-test) supporting increased oligodendrogenesis in IκBα-dn mice already at 6 weeks post-SCI. N = 4 animals per group. NG2, nerve/glial antigen 2.