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. 2020 Nov 13;8:564351. doi: 10.3389/fcell.2020.564351

FIGURE 7.

FIGURE 7

LRP1 does not affect OPC proliferation in vitro. (A–B″) Tat-Cre-treated OPCs cultured from the cortex of early postnatal control (Pdgfrα-histGFP) and Lrp1-deleted (Pdgfrα-histGFP :: Lrp1fl/fl) mice were immunolabeled to detect PDGFRα (red), LRP1 (blue), and GFP (green). (C) Quantification of the proportion (%) of control and Lrp1-deleted OPCs that express LRP1 48 h after TAT-Cre treatment (mean ± SEM, n ≥ 3 independent cultures per genotype; unpaired t-test, ****p < 0.0001). (D,E) Tat-Cre-treated OPCs from control and Lrp1-deleted mice exposed to EdU for 10 h and immunolabeled to detect GFP (green), LRP1 (red), and EdU (blue). (F) Quantification of the proportion (%) of control and Lrp1-deleted OPCs that become EdU-labeled over a 10-h period (mean ± SEM, n ≥ 5 independent cultures per genotype; unpaired t-test, p = 0.3). (G–I′) Compressed confocal z-stack showing OPCs cultured from control mice that were exposed to EdU and either vehicle (MilliQ water; G,G′), 20 nM tPa (H,H′) or 60 nM *α2M (I,I′) for 10 h, before being processed to detect EdU (red) and PDGFRα (green). (J) Quantification of the proportion (%) of control OPCs that incorporated EdU when treated with vehicle, tPa or *α2M for 10 h (mean ± SEM, n ≥ 4 independent cultures; 1-way ANOVA: Treatment F (2, 9) = 0.42, p = 0.66). Scale bars represent 17 μm. DIV = days in vitro; tPA = tissue plasminogen activator; *α2M = activated α-2 macroglobulin.