Supplementary Figure 6: OPC perivascular clustering in remyelination impairs their recruitment into lesions. | Nature Neuroscience

Supplementary Figure 6: OPC perivascular clustering in remyelination impairs their recruitment into lesions.

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

Supplementary Figure 6

(a) Double staining for PDGFRα+ OPCs and CD31+ vasculature shows OPC distribution before (0dpl ‘No lesion’ top row) and after lysolecithin lesioning at 3 days post lesioning (3dpl) in dorsal funiculus of the spinal cord in APCfl/fl control, Olig2cre:APCfl/fl and PDGFRα-creERT2:APCfl/fl mice. There are reduced OPC numbers (stars) at early 3dpl time points in spinal cord lesion centers in both PDGFRα-creERT2:APCfl/fl and Olig2cre:APCfl/fl mice. (b) Quantification of number of PDGFRα+ OPCs in lesion centers in unlesioned (0 days) and 3 days post lesioning (3dpl) spinal cord dorsal funiculus lesions in APCfl/fl (white bars) and Olig2cre:APCfl/fl (grey bars) mice (n=4 animals; 3d APC fl/fl vs. 3d Olig2 cre:APC fl/fl **p = 0.0013). Data were analyzed by unpaired two-sided Student’s t test. (c) Quantification of number of PDGFRα+ and Olig2+ cells in lesion centers in unlesioned (0 days) and 3 days post lesioning (3dpl) spinal cord dorsal funiculus lesions in APCfl/fl (white bars) and PDGFRα-creERT2:APCfl/fl (grey bars) mice (n=4 animals; PDGFRα: 3d APCfl/fl vs. 3d PDGFRα-creERT2:APC fl/fl ***p = 0.0003; Olig2: 3d APCfl/fl vs. 3d PDGFRα-creERT2:APC fl/fl **p = 0.0031). Data were analyzed by unpaired two-sided Student’s t test. (d) Quantification of number of PDGFRα+ OPCs on blood vessels at lesion edges in unlesioned (0 days) and 3 days post lesioning (3dpl) spinal cord dorsal funiculus lesions in APCfl/fl (white bars) and PDGFRα-creERT2:APCfl/fl (grey bars) mice (n=4 animals; 3d APCfl/fl vs. 3d PDGFRα-creERT2:APCfl/fl *p = 0.0215). Data were analyzed by unpaired two-sided Student’s t test. (e-h) Recruitment deficits into lesions in mice with Wnt-hyperactive OPCs do not seem to be due to differences in OPC proliferation. (e) Double staining for PDGFRα+ OPCs and Ki67 at 3 days post lesioning (3dpl) in dorsal funiculus of the spinal cord in APCfl/fl and PDGFRα-creERT2:APCfl/fl mice, quantified in (f) as percentage of PDGFRα+ cells that are also Ki67+ in lesion centers at 3dpl (n=4 animals; 0d APCfl/fl vs. 0d PDGFRα-creERT2:APCfl/fl, ns p = 0.3234; 3d APCfl/fl vs. 3d PDGFRα-creERT2:APCfl/fl, ns p = 0.9845). Data were analyzed by unpaired two-sided Student’s t test. (g-h) OPCs in vitro from APCfl/fl and Olig2cre:APCfl/fl proliferate to a similar extent (g), quantified in (h) as percentage of PDGFRα+ cells that are also Ki67+ (n=4 independent experiments; APCfl/fl vs. Olig2-cre:APCfl/fl, ns p = 0.9235). Data were analyzed by unpaired two-sided Student’s t test. Scale bars, 60 μm (a, e), 30 μm (g). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Values are mean ± s.d.

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