Fig. 2

Myrf ICKO mice generate few new oligodendrocytes in response to SCI. Overview of OLIG2 staining at injury epicenter in a control and b Myrf ICKO mice at six WPI. Boxes are approximate areas where c and d were imaged. c, d Example high magnification representative images of the ventrolateral white matter stained with PDGFRα, OLIG2, CC1, and EdU in control and Myrf ICKO mice. Single channel images are displayed separately on the right. Yellow arrows indicate oligodendrocytes lacking EdU (OLIG2+ CC1+ EdU-negative), which are likely spared oligodendrocytes, while white arrows indicate new oligodendrocytes (OLIG2+ CC1+ EdU+) and blue arrows indicate OPCs (OLIG2+ PDGFRα+ EdU±). There are very few new oligodendrocytes following SCI in Myrf ICKO. e Quantification demonstrates control mice have a higher density of new oligodendrocytes (CC1+ OLIG2+ EdU+) (df = 15, t = 9.224, P < 0.001, Student’s t test) and total oligodendrocytes (CC1+ OLIG2+) (df = 15, t = 5.570, P < 0.001, Student’s t test) compared to Myrf ICKO animals. f Distribution of newly generated cells at different distances from lesion epicenter (OLIG2+ CC1+ EdU+). At all distances, control mice have more new oligodendrocytes relative to Myrf ICKO mice (multiple Student’s t test with Holm-Šídák correction, epicenter t = 4.100, P = 0.001, all others distances P < 0.001). g Quantification of the density of OPCs that have proliferated (PDGFRα+ OLIG2+ EdU+) and total density of OPCs (PDGFRα+ Olig2+) indicate there is no statistical difference between Myrf ICKO and controls (total OPC density: df = 15, t = 1.535, P = 0.146; proliferative OPC density: df = 15, t = 1.267, P = 0.225, Student’s t tests). ^**P ≤ 0.01 ^***P ≤ 0.001. Scale bars = 100 µm (a, b), 20 µm (c, d). Error bars are mean ± SEM