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. 2017 Feb 9;8(3):685–700. doi: 10.1016/j.stemcr.2017.01.007

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© 2017 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Dynamics of Cells of the Oligodendroglial Lineage after Demyelination in the Aging CC

(A and B) Microphotographs of the CC from young (A) and aging (B) mice at 15 dpl after immunostaining for OLIG2, EYFP, and PCNA; a dividing pOPC and a dividing sezOPC are shown in the blown-up rectangle at the right end of (A), with an arrowhead and an arrow, respectively. A non-dividing sezOPC is shown in the blown-up rectangle at the right end of (B) with an arrow.

(C) Microphotographs of the CC from an aged mouse at 7 dpl after immunostaining for OLIG2, EYFP, and PCNA (a sezOPC is indicated by the arrow).

(D) Graph showing the density of OLIG2+ cells of parenchymal origin in control mice of different ages and at different dpl in young and 14-month-old CC, as well as at 7 dpl in the 25-month-old CC (^∗p < 0.05 compared with control levels of the young adult mice; ^#p < 0.05 compared with control levels in the 14month-group; ^$p < 0.05 compared with control levels in the 25 month group; two-way ANOVA, followed by the Scheffe post hoc analysis; error bars, SEM).

(E) Graph showing the respective information for the SEZ-derived component of the CC (^∗p < 0.05 compared with control levels of the young adult mice; ^#p < 0.05 compared with control levels in the 14 month group; ^$p < 0.05 compared with control levels in the 25 month group; two-way ANOVA followed by the Scheffe post hoc analysis).

(F) Graph showing the fraction of each population of OPCs that is proliferating in control mice of different ages and after demyelination. Note the absence of proliferating sezOPCs in the 14 and 25 month CC and the significant decrease in proliferating pOPCs in the 25 month CC (^∗p < 0.05 compared with control levels of the same age group in sezOPCs; ^#p < 0.05 compared with control levels in the same age group in pOPCs; ^$p < 0.05 compared with control levels in the young adult mice for pOPCs; two-way ANOVA followed by the Scheffe post hoc analysis).

(G) Graphs showing the density of parenchymal and SEZ-derived OPCs and oligodendrocytes in controls and 7 dpl 24-month-old mice. At 7 dpl the overall parenchymal OLIG2+ cell numbers are significantly lower compared with control mice (indicated by the bracket). Numbers of pOPCs (OLIG2+/CC1−) are at normal levels, while oligodendrocytes of parenchymal origin (CC1+) are significantly depleted. The total number of SEZ-derived cells is significantly increased at 7 dpl (indicated by the brackets), with sezOPCs being significantly increased and SEZ-derived oligodendrocytes being at normal levels (^∗p < 0.05, using Student's t test). Error bars depict the SEM. Scale bars, 50 μm (A), (B); 20 μm in magnifications and in (C). n = 6 mice per time point for young-adult and 14-month-old mice, n = 4 for 25-month-old mice.