Supplementary Figure 2: OPC recruitment into murine lysolecithin spinal cord remyelinating lesions. | Nature Neuroscience

Supplementary Figure 2: OPC recruitment into murine lysolecithin spinal cord remyelinating lesions.

From: Aberrant oligodendroglial–vascular interactions disrupt the blood–brain barrier, triggering CNS inflammation

Supplementary Figure 2

(a) Double staining for PDGFRα+ OPCs and CD31+ vasculature shows OPC distribution before (0dpl ‘No lesion’) and after lysolecithin lesioning at 1day post lesioning (1dpl), 2dpl and 3dpl in dorsal funiculus of the spinal cord in mice. OPCs are eliminated from the lesion at 1dpl, with recruitment of small numbers back into the lesion by 2dpl. (b) Double staining for Ki67 and PDGFRα to mark proliferating OPCs in and around mouse spinal cord dorsal funiculus lesions at these same time points. (c) Quantification of OPC proliferation outside the lesion (dorsal funiculus outside the lesion) in unlesioned (0d) dorsal funiculus spinal cord and at 1, 2, 3, 5, 7 and 14dpl after lysolecithin lesioning, showing total number of PDGFRα cells per mm2 (black lines and black stars; n=6 animals at each time point; all statistical analyses compared with 0d, 1d vs. 0d ns p = 0.9705, 2d vs.0d ns p = 0.0691, 3d vs. 0d **p = 0.0054, 5d vs. 0d ns p = 0.0613, 7d vs. 0d ns p = 0.7910, 14d vs. 0d ns p = 0.5827) and those that are Ki67+ (red lines and red stars; n=6 animals at each time point; all statistical analyses compared with 0d, 1d vs. 0d ns p = 0.9314, 2d vs. 0d ****p = 3.04 E-9, 3d vs. 0d ****p = 2.14 E-8, 5d vs. 0d ****p = 3.70 E-6, 7d vs. 0d *p = 0.0141, 14d vs. 0d ns p = 0.9999). Data were analyzed by unpaired two-sided Student’s t test. (d) Quantification of OPC proliferation inside the lesion in dorsal funiculus spinal cord at 1, 2, 3, 5, 7 and 14dpl after lysolecithin lesioning, showing total number of PDGFRα cells per mm2 (black lines and black stars; n=6 animals at each time point; all statistical analyses compared with 0d, 1d vs. 0d *p = 0.0322, 2d vs. 0d ns p = 0.9195, 3d vs. 0d ****p = 3.96 E-8, 5d vs. 0d ****p = 2.25 E-8, 7d vs. 0d ****p = 2.39 E-5, 14d vs. 0d ****p = 1.74 E-4) and those that are Ki67+ (red lines and red stars; n=6 animals at each time point; all statistical analyses compared with 0d, 1d vs. 0d ns p = 0.9715, 2d vs. 0d *p = 0.0204, 3d vs. 0d ****p = 3.42 E-16, 5d vs. 0d ****p = 6.95 E-17, 7d vs.0d ****p = 1.48 E-7, 14d vs. 0d ns p = 0.0668). Data were analyzed by unpaired two-sided Student’s t test. (e) Analysis of OPCs with or without leading processes and their association with vasculature (‘On’ vessel or ‘Off’ vessel) in unlesioned mouse spinal cord dorsal funiculus or in dorsal funiculus outside a 2dpl lysolecithin lesion (n=6 animals; the percentage of total OPCs on blood vessel: Unlesioned On vs. 2d On, white bars and black stars, ****p = 1.36 E-5; the percentage of OPCs on blood vessel with leading process: Unlesioned On w/ leading process vs. 2d On w/ leading process, red bars and red stars, ****p = 2.11 E-9; the percentage of total OPCs NOT on the blood vessel: Unlesioned Off vs. 2d Off, white bars and black stars, ****p = 1.66 E-5; the percentage of OPCs NOT on the blood vessel with leading process: Unlesioned Off w/ leading process vs. 2d Off w/ leading process, red bars, ns p = 0.437). Data were analyzed by unpaired two-sided Student’s t test. Scale bars, 40 μm (a, b). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Values are mean ± s.d.

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