Fig. 7

Traumatic brain injury induces senescence in OLs and myelin loss in the impact area. a and b NF-ĸB is activated in O4⁺OLs post TBI as determined by FACS analysis of O4⁺ OLs isolated from sham and TBI treated ĸ-EGFP reporter gene mice. A significant fraction of O4⁺ cells from TBI-treated ĸ-EGFP mice show eGFP expression 14 days post TBI (sham 1.75 ± 0.15%, TBI: 5.85 ± 1.58% n = 4). c and d A significant higher percentage of X-gal positive cells was detected in O4.⁺ OLs isolated from the ipsilateral hemisphere 14 dpi post TBI indicating senescence associated ß-galactosidase activity compared to uninjured contralateral hemisphere. Black arrows mark blue colored X-gal positive cells (contra: 5.38 ± 0.37%, ipsi: 11.89 ± 2.04%, n = 4). e Immunofluorescence and LFB analysis revealed strong loss of myelin basic protein (MBP) and reduced LFB staining within the insult area as indicated by dotted lines (3 dpi). f In contrast, the NF-ĸB target gene and SASP factor Lcn2 is found upregulated in the insult region as determined by immunofluorescence staining (3 wpi post TBI). Dotted lines indicate the TBI insult area. Data are shown as mean ± SEM. Grey bar, sham/contra; blue bar, TBI/ipsi. Statistical analysis: Two-tailed Mann–Whitney-U Test, (*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 NS, non-significant (p > 0.05))